Publication for Il13 and Il9

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression		 CoexViewer
mmu Il13 interleukin 13 16163 [link]
mmu Il9 interleukin 9 16198

Pubmed ID Priority Text
14970180 0.98 IL-9, IL-13, GM-CSF, TNF-alpha, regulated on activation, normal T cell expressed and secreted (RANTES), and macrophage inflammatory protein (MIP)-1alpha, suggesting their relevant role in induction of bronchial asthma.
0.98 IL-9 and IL-13), TNF-alpha (not depicted), GM-CSF, and chemokines.
0.98 IL-9, IL-13, RANTES, and MIP-1alpha upon stimulation with Ag, IL-2, and IL-18 (Fig. 3 A).
0.97 IL-9, and IL-13) and GM-CSF are principally responsible for inducing bronchial asthma.
0.97 IL-9 and IL-13 induce mucus production by causing goblet cell hyperplasia.
0.97 IL-9, IL-13, etc.), when they are stimulated with IL-2 and IL-18 without TCR engagement, although they have the potential to produce a large amount of IFN-gamma in response to IL-12 and IL-18.
0.97 IL-9, and IL-13.
0.97 IL-13 (Fig. 6 A), Ag plus IL-18-stimulated Th1 cells produced a variety of cytokines including IL-9, GM-CSF, RANTES, and MIP-1alpha.
0.97 IL-9, IL-13, GM-CSF, TNF-alpha, RANTES, and MIP-1alpha.
0.97 IL-9, IL-13, GM-CSF, RANTES, and MIP-1alpha when they are stimulated with Ag, IL-2, and IL-18 in vitro (Figs. 3 A and 6 C).
0.97 IL-9, IL-13, GM-CSF, TNF-alpha, RANTES, and MIP-1alpha, providing a potential therapeutic target molecule for the establishment of the treatment for allergic disorders.
0.96 IL-9, IL-13, granulocyte/macrophage colony-stimulating factor, tumor necrosis factor alpha, regulated on activation, normal T cell expressed and secreted, and macrophage inflammatory protein 1alpha upon stimulation with Ag, IL-2, and IL-18 in vitro.
0.96 IL-9, IL-13, GM-CSF, and some chemokines from Th1 cells in induction of both severe airway inflammation and AHR.
0.96 IL-9, IL-13, and GM-SCF.
0.96 IL-9, IL-13, IFN-gamma, and GM-CSF but not IL-4 production (Fig. 6 C).
0.94 IL-9, and IL-13 in response to IL-18 (Fig. 3 A).
0.94 IL-9, IL-13, GM-CSF, RANTES, and MIP-1alpha production from OVA-specific Th1 cells.
0.94 IL-9, IL-13, and GM-CSF production from IFN-gamma+ Th1 cells.
0.94 IL-9, IL-13, RANTES, and MIP-1alpha in normal BALB/c mice.
0.93 IL-9, IL-13, TNF-alpha, GM-CSF, RANTES, eotaxin, MIP-1alpha, and IFN-gamma in the culture supernatant of Th1 cells because they are reported to be deeply involved in induction of bronchial asthma.
0.93 IL-9, IL-13, TNF-alpha (not depicted), and GM-CSF in Th1 cells (Fig. 3 A).
0.92 IL-9, IL-13, and chemokines when they are stimulated with Ag, IL-2, and IL-18 in vitro, it might be important to point out the possibility that administration of memory-type Th1 cells could mimic the mixed asthma responses that are attainable by activation of both Th1 and Th2 cells.
0.90 IL-9, IL-13, and GM-CSF.
0.89 IL-9, and IL-13 but not IFN-gamma, and Th1 cells produced IFN-gamma but not Th2 cytokines (Fig. 3 A).
21983833 0.98 IL-9 production via neutralizing antibodies substantially reduced IL-13 and IL-5, suggesting that ILC provide the missing link between the well-established functions of IL-9 on the regulation of TH2 cytokines and responses.
0.98 IL-9 in lung physiology is the induction of mucus production, goblet cell hyperplasia and other features of airway remodelling, functions that were also attributed to IL-13 as well as IL-5 via the regulation of eosinophils.
0.98 IL-9 protein expression in favour of IL-5 and IL-13 expression.
0.98 IL-9 markedly increased the ILC production of IL-5, IL-6 and IL-13 (Fig. 7f), suggesting that IL-9 could provide an additional activation signal important for cytokine expression.
0.98 IL-9-neutralized mice, IL-5 and IL-13 expression was reduced to less than half of the levels recovered from isotype control treated mice, indicating that IL-9 indeed has an additive effect on IL-5 and IL-13 expression in vivo (Fig. 7g).
0.98 IL-9 has a feedback effect on ILC, resulting in increased production of IL-5 and IL-13.
0.98 IL-9 induced airway inflammation is observed in IL-9 transgenic mice, but is ablated if IL-9 transgenic mice are backcrossed onto an IL-13 deficient background, indicating that IL-9 acts via expression of IL-13.
0.98 IL-13 and IL-5 production in ILC upon IL-9 stimulation, suggesting that IL-9 mediated airway inflammation may be the result of enhanced IL-13 and IL-5 expression from ILC.
0.97 IL-9 production by ILC was dependent on IL-2 from adaptive immune cells and was rapidly lost in favor of other cytokines, such as IL-13 and IL-5.
0.97 IL-13, in CD25+ ILC and especially in eYFP+ ILC from the IL-9 reporter mice (Fig. 3d), emphasising their activated state.
0.97 IL-9 during papain-induced lung inflammation resulted in reduced levels of IL-13 and IL-5 when analysed 3 days after challenge.
0.97 IL-9 expression might be the missing link for sustained IL-13 expression in nuocytes and ILC in general.
0.96 IL-9 from ILC and a potential involvement of IL-9 in allergic lung diseases via the promotion of IL-5 and IL-13 production in ILC.
0.96 IL-13 are linked to IL-9 and IL-9 induction requires IL-2, lack of IL-2 signaling might also affect the amounts of IL-5 and IL-13.
0.95 IL-9 was found to facilitate IL-5 and IL-13 production from ILC, while neutralisation of IL-9 reduced the levels of IL-5 and IL-13 after papain challenge.
0.95 IL-9, IL-5 and IL-13 were detectable after CD4+ T cell transfer, ILC transfer resulted in substantially elevated levels of IL-9, IL-5 and IL-13 (Fig. 6e).
0.92 IL-9 and IL-13 expression stems almost exclusively from ILC (Fig. 6d).
0.87 IL-9 but sustained IL-5 and IL-13 production in ILCs
0.86 IL-9 effects on intestinal mucosa were reported to be IL-13 dependent.
0.85 IL-13 by IL-25 or IL-33, IL-9 was not directly induced by the latter two cytokines, but instead depended on IL-2.
0.62 IL-9 during papain-induced lung inflammation we performed intracellular cytokine staining for IL-9 and IL-13 in ILC and CD4+ T cells.
29132961 0.98 IL9 and IL13 but not IL5 in bronchoalveolar lavage (BAL).
0.98 IL9+ and IL13+ ILC2s and mast cells, and leads to the development of chronic experimental asthma.
0.98 IL9+ and IL13+ ILC2s in the airways and an increase in mast cells.
0.98 IL9 was previously shown to exert an autocrine effect and amplified IL13 production, which sustained inflammation by inducing IL33 and TSLP production by airway epithelial cells.
0.97 IL13+ ILC2s, the emergence of a TSLP-R+ IL9+ ILC2 population and an increase in intraepithelial mast cells in the lung.
0.97 IL13 and IL9 were elevated in the lung (online repository figure E4 A & B) and in BAL from the chronic asthma model (Figure 3C & D).
0.97 IL9+ and IL13+ ILC2s and intraepithelial mast cells.
0.96 IL9+ and IL13+ ILC2 subpopulations
0.96 IL9+ and IL13+ ILC2s and the expression of IL9 and IL13 in the airways
0.95 IL9 and IL13 stimulate mucus production.
0.95 IL9 and IL13level in BAL (Figure 7 A-C).
0.93 IL13+ and IL9+ ILC2s as compared to WT mice (Figure 2D & E).
0.91 IL9, IL13 and TSLP are elevated in the airways from ST2 KO mice
0.90 IL9+ and IL13+ ILC2s in the lung.
0.82 IL9+ and IL13+ ILC2s are elevated in ST2 KO mice
0.80 IL9+ILC2s and IL13+ILC2s (Figure 6A-E).
0.74 IL13+ and IL9+ ILC2s in this group.
22346732 0.98 IL-9, IL-10, IL-13, IL-17A, and IL-22, while IFN-gamma production is diminished in Il15 L117P iNKT cells (Figure 1).
0.98 Il13 expression but also in Il9, Il17a, and Il22 expression by IL-25-treated CD4+ IL-17RB+ iNKT cells.
0.98 IL-9, IL-10, IL-13, IL-17A, and IL-22 cytokines by both thymic or splenic CD4+ IL-17RB+ iNKT cells in response to IL-25 was completely abrogated, indicating E4BP4 turned out to be an intrinsic regulator of IL-25-mediated production, not only of IL-10 and IL-13 but also of IL-9, IL-17A, and IL-22.
0.98 IL-13 but also IL-9, IL-17A, and IL-22 were attenuated in the absence of E4bp4, recently defined as a transcription factor that regulates IL-10 and IL-13 production by CD4+ T cells and iNKT cells, suggesting that E4BP4 also controls IL-25-mediated production of IL-9, IL-17A, and IL-22.
0.98 IL-9, IL-10, IL-13, IL-17A, and IL-22 expression by genetic/epigenetic regulation in CD4+ IL-17RB+ iNKT subtypes.
0.97 IL-13), TH9 (IL-9 and IL-10), and TH17 (IL-17A and IL-22) cytokines in response to IL-25 in an E4BP4-dependent fashion, whereas CD4- IL-17RB+ iNKT cells are a retinoic acid receptor-related orphan receptor (ROR)gammat+ subset producing TH17 cytokines upon stimulation with IL-23 in an E4BP4-independent fashion.
0.97 IL-9, IL-10, IL-13, IL-17A, and IL-22, was severely impaired in the Il17rb -/- mice.
0.97 IL-9, IL-10, IL-13, IL-17A, and IL-22 Cytokines by CD4+ IL-17RB+ iNKT Cells in Response to IL-25
0.97 IL-13 and IL-4 but also IL-9 and IL-10 along with IL-17A and IL-22 in response to IL-25 in an E4BP4-dependent fashion.
0.95 IL-9, IL-10, and IL-13 among TH2 cytokines and IL-17A and IL-22 TH17-type cytokines.
0.94 IL-13 and IL-4 but also IL-9 and IL-10 from CD4+ IL-17RB+ iNKT cells, which can thus be characterized as iNKT-TH2 and iNKT-TH9 cells.
0.93 Il9, Il10, Il13 (unpublished data), Il17a, or Il22 mRNA (Figures 3B, S5B, S10B) in the steady state, even though these cytokines are immediately produced after activation by alpha-GalCer, similar to cases of IFN-gamma from IL-17RB- iNKT cells.
0.92 IL-9, IL-10, and IL-13, but also of TH17 cytokines IL-17A and IL-22 in Il17rb -/- iNKT cells, but not in Il15 L117P iNKT cells in the spleen (Figure 1C and 1D), even though the number of iNKT cells were only slightly decreased in Il17rb -/- (see Figure 1A).
0.84 IL-9, IL-10, IL-13, IL-17A, and IL-22) in the BAL fluid was detected in this experiment (Figure 7D).
0.83 IL-9, IL-10, IL-13, IL-17A, and IL-22 was impaired in the Il17rb -/- but not in the Il15 L117P iNKT cells, similar to what we had observed in the spleen and liver (Figure S3).
0.68 IL-9, IL-10, and IL-13 were mainly produced by the CD4+ IL-17RB+ iNKT cells.
25786692 0.98 IL-9 acts on mast cells, epithelial cells and smooth muscle cells to promote production of cytokines and chemokines such as IL-8, IL-13 and eotaxin, which enhance recruitment and activation of neutrophils, eosinophils and mast cells in allergic inflammation.
0.98 IL-9 has been shown to induce airway remodeling in an IL-13 dependent manner, placing IL-9 'upstream' of IL-13 in these disease models.
0.98 IL-9 and IL-13 production by T cells early in the lung hypersensitivity response, which may shape the ensuing allergic pathology.
0.98 IL-9 and IL-13 was highly induced after 2 weeks of papain exposure, and DR3-deficient mice were defective in induction of both IL-9 and IL-13 mRNA, with the reduction in IL-9 even more pronounced than that in IL-13 (Figure 2F).
0.98 IL-9 production in T cells cultured for 3 days under non-polarizing Th0, Th1 or Th2 conditions, and TL1A did not enhance the production of cells expressing IL-4 or IL-13 under Th2 conditions (Supplemental Figure 3A), suggesting that the TGFbeta and IL-2 included in iTreg polarization conditions are important for the ability of TL1A to induce IL-9 production.
0.97 IL-9, TL1A enhanced the production of IL-2, IL-3, IL-10, IL-13, and GM-CSF by purified T cells activated under Th9 conditions (Figure 3I, top panel).
0.95 IL-9 and IL-13 upregulation appeared strongest in Th9 and iTreg conditions in purified T cell culture.
0.95 IL-9 and IL-13 production in T-cell driven allergic lung inflammation
0.94 IL-9, IL-13 and IL-2 mRNA were significantly reduced in Ova-treated recipients of Tnfrsf25-/- OT-II T cells compared with mice that received WT OT-II T cells (Figure 7E).
0.94 IL-9 and IL-13 production by T cells in response to an inhaled allergen
0.93 IL-9 and IL-13 in allergic airway disease
0.93 IL-13 and IL-9 were induced by TL1A (Figure 3C).
0.91 IL-9 or IL-13 were strikingly reduced in DR3 deficient mice (Figure 2G).
0.90 IL-9 mRNA was elevated on day 16, one day after the last challenge with Ova, whereas IL-13 production was higher at day 18.
0.89 IL-9 and IL-13 secreting cells increased approximately 10-fold in Ova-sensitized WT mice compared to PBS-sensitized controls, whereas no such changes in cells secreting IL-9 nor IL-13 could be seen in Tnfrsf25-/- mice.
0.73 IL-9 mRNA was not induced at either time point, and IL-13 was significantly reduced at day 18 (Figure 1B).
26129648 0.98 IL-9 program in ILC2s, and autocrine IL-9 promotes rapid IL-5 and IL-13 production required for optimal epithelial responses in the conducting airways.
0.98 IL-9 requires IRF4 and acts in an autocrine manner to optimize IL-5 and IL-13 production.
0.98 Il13 and of IL-13 target genes known to be expressed in lung epithelial cells to promote mucus production and tissue repair, including Muc5ac, Clca3, and Tff2, were significantly reduced in mice lacking IRF4 or IL-9 (Figure 6c).
0.98 IL-9 from lung ILC2s is generated in a rapid, IRF4-dependent manner in vivo and is required for optimal ILC2 elaboration of IL-5 and IL-13, which drives subsequent eosinophilia and supports epithelial defense and repair.
0.98 IL-9 program in ILC2s, in which IL-9 sustained autocrine amplification of IL-5 and IL-13 production.
0.98 IL-9, IL-13-dependent expression of epithelial genes involved in barrier responses, including increases in mucus and enzymatic chitinase and promotion of repair, was abrogated.
0.97 IL-9 rapidly generates IL-5, IL-13 and subsequent conducting airway proteins that drive tissue defense and repair.
0.97 IL-9 to late lung repair and adaptive Th9-mediated worm immunity, our data demonstrate a novel role for IL-9 in acute stabilization of mucosal homeostasis, as IL-13-mediated epithelial responses were highly attenuated in its absence.
0.96 IL-9, IL-5, and IL-13 in BAL fluid 1 day after infection (Figure 5e), and ILC2s sorted from the lungs of these mice expressed these cytokines when cultured overnight without further stimulation (Supplementary Figure S6c).
0.96 IL-9 expression to epithelial gene transcription via IL-13 from hematopoietic cells.
0.94 IL-9, IL-5, and IL-13 in a manner identical to that of Il99er/9er cells; diminished IL-5 and IL-13 expression in Irf4-/- ILC2s could be rescued by addition of IL-9 (Figure 4e).
0.86 IL-9 also produced significantly less IL-5 or IL-13 in overnight ex vivo cultures (Figure 6b).
0.85 IL-9-deficient mice had reduced induction of Il13 transcripts as compared with wild-type mice, although induction of Il5 was not affected under these conditions (Figure 5b).
0.71 IL-13, and IL-9, the addition of 0.1 ng ml-1 TSLP significantly increased production; no cytokines were detected when ILC2s were cultured with TSLP alone, even at 100-fold higher concentrations (Figure 3a).
31511826 0.98 IL-9, IL-10, and IL-13).
0.97 IL-9, IL-10, and IL-13 expression in CD4+ T cells.
0.97 IL-13, and IL-10 as well as of IL-9 on mRNA and protein level in T cells derived from KSRP-/- mice in the course of CAIA progression.
0.97 IL-13 mRNA for rapid degradation by ARE-binding RBPs (RBP TTP, AUF1, and HuR) has been documented, much less is known about the mechanisms of the posttranscriptional regulation of IL-5 and IL-9 mRNA expression.
0.97 IL-9, IL-10, IL-13, and IFN-gamma in T cells.
0.97 IL-13, IL-9, and IFN-gamma cytokine production in T cells and enhance CD4+ T cell proliferation upon polyclonal stimulation.
0.96 IL-9, IL-10, and IL-13 were observed to be increased compared to those of the control group.
0.96 IL-9, IL-10, and IL-13 in T cells derived from KSRP+/+ mice during CAIA disease progression.
0.93 IL-9, IL-10, and IL-13 in CD4+ T cell RNA samples isolated from KSRP-/- mice in comparison to the WT control group (Figure 3(b)).
0.89 IL-9, IL-10, and IL-13), we detected an increased production over time.
0.85 IL-13, as well as of IL-9 and IL-10 compared to control cells (Figures 1 and 2).
0.84 IL-9, IL-10, IL-13, or IFN-gamma mRNA and protein expression remains to be elucidated.
0.80 IL-9, IL-10, IL-13, or IFN-gamma mRNA expression via direct or indirect mechanisms.
0.56 IL-13 3'-UTR but not to the IL-5 and IL-9 3'-UTR (Figure 6).
32103032 0.98 IL-13 (two cytokines implicated in asthma) but not IL-5, IL-9 or GM-CSF in response to IL-33.
0.98 IL-9, IL-13 and GM-CSF in response to IL-33 treatment.
0.98 IL-9, IL-13 and GM-CSF in IL-33 stimulated ILC2s.
0.97 IL-9, IL-13 and GM-CSF by ILC2 in response to IL-33, with inhibition of p38 having the greatest effect.
0.97 IL-9, IL-13 and GM-CSF, and the amount of secreted cytokine present in the media increases over 3 to 5 days of stimulation.
0.97 IL-9, IL-13 and GM-CSF in response to IL-33 (Fig. 3A).
0.97 IL-9, IL-13 and GM-CSF (Fig. 4).
0.96 IL-13 were regulated by the p38alpha activated kinases MK2 and 3, while IL-5, IL-9 and GM-CSF production were independent of MK2/3.
0.95 IL-9 and IL-13 (Supplementary Fig. 2).
0.95 IL-9, IL-13 and GM-CSF while MK2/3 and mTOR selectively drive IL-6 and IL-13 production.
0.94 IL-13 production in response to IL-33 but had little effect on IL-5, IL-9 and GM-CSF induction.
0.91 IL-9 and IL-13 following IL-33 stimulation.
0.89 IL-9, IL-13 and GM-CSF (Fig. 5B-F).
0.79 IL-9, IL-13 and GM-CSF in response to IL-33, however the kinetics of cytokine production was in general faster than in the FACS sorted cells (Fig. 3B).
24138883 0.98 IL-9 expression in both mucosal tissues and secondary lymphoid organs, which preceded IL-4, IL-5, and IL-13 expression at these sites.
0.98 IL-13 expression, which is significantly reduced in the absence of IL-9 (Figure 2B), increased to levels comparable to wildtype mice in the small intestine upon reintroduction of Th9 cells (Figure 5B).
0.98 IL-9 deficient mice, we found that IL-9 promotes IL-5 and IL-13 expression and increases basophilia, eosinophilia and mast cell numbers in parasite-targeted tissues, ultimately leading to efficient worm expulsion.
0.97 IL-9 expression was strictly transient, suggesting a very tight control in the expression of this cytokine in vivo, and was detected earlier than IL-4, IL-5 and IL-13 in all tissues examined (Figures 1E-1H).
0.97 Il13 mRNA expression was severely impaired in lung and small intestine of IL-9 deficient mice at day 7 p.i (Figure 2B).
0.97 IL-9 is sufficient to decrease worm loads and significantly increase IL-13 and IL-5 expression in small intestine.
0.96 IL-9 and IL-13 amounts, eosinophilia, mastocytosis, basophilia, goblet cell metaplasia, and immunoglobulin E (IgE) production, the pathways responsible for initiating these responses remain controversial.
0.96 IL-9 is necessary for IL-5 and IL-13 induction, eosinophilia, basophilia and worm clearance in vivo
0.95 IL-9 expressing ILC2 cells have also been observed in a papain-induced lung inflammation model; however, this expression was transient and transitioned to IL-5 and/or IL-13 expression over time.
0.94 IL-9 expression precedes IL-4, IL-5 and IL-13 during N. brasiliensis infection
0.86 IL-9 expression also preceded that of IL-4, IL-5 and IL-13 (Figure S1).
0.85 IL-9 expression precedes IL-4, IL-5 and IL-13 in vivo
31937554 0.98 IL-9 and IL-13 are associated with eosinophil recruitment and survival in the lungs.
0.98 IL-9 and IL-13 are responsible for eosinophil infiltration into lung based on ours and others observations.
0.98 IL-9 and IL-13, and eosinophil infiltration into the lungs, both of which augments lung inflammation after HS.
0.97 IL-9+ ILC2s and IL-13+ ILC2s in WT mice (figure 6A-C).
0.97 IL-9 and IL-13 in plasma were markedly increased at 24 hours after rHMGB1 treatment (online supplementary figure 5D) or HS (figure 6G).
0.97 IL-9 and IL-13, mediates host protection through reducing tissue inflammation and enhancing tissue repair.
0.96 IL-9 and IL-13 in plasma after HS as compared with WT mice (figure 6G).
0.95 IL-9+ ILC2s and IL-13+ ILC2s (figure 6A-C).
0.95 IL-9 and IL-13 production in plasma at 24 hours post-HS (figure 6H).
0.88 IL-9+ ILC2s and IL-13+ ILC2s in the lungs (online supplementary figure 5A-C) but did not increase IL-4+ ILC2s (data not shown).
0.85 IL-9+ ILC2s and IL-13+ ILC2s at 24 hours after HS (figure 6D-F).
0.81 IL-13 were also markedly increased at 24 hours after HS (figure 1C) while plasma concentrations of IL-4 and IL-9 did not show statistic differences between the groups of HS and healthy controls (data not shown).
26410628 0.98 IL-9 (~2.0 pg/mL per cell) and other Th2 cell-associated cytokines, including IL-4 and IL-13, in lesser amounts after PMA plus Ionomycin stimulation (Figure 2B).
0.97 IL-9-producing mucosal mast cells (MMC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell protease-1 (MCPt-1) in response to antigen and IgE complex crosslinking, respectively.
0.97 Il13 (>106 fold), and transcription factor Gata3 (>103 fold) and Rora (>104 fold), and moderate amounts of Il9 (<103 fold) transcripts (Figure 2E and data not shown).
0.97 IL-9 and IL-13 in response to IL-33, and MCPt-1 protein and histamine in response to IgE-bound FcepsilonR complex cross-linking by antigens.
0.96 IL-9 producers were the beta7integrinlo subset of Lin-GFPhiIL-17RB-c-Kit+ST2+ cells, while both beta7integrinhi and beta7integrinlo subsets could produce IL-13 (Figure 2D).
0.95 Il13 transcript (>104 fold), but only beta7integrinloLin-GFPhiIL-17RB-c-Kit+ST2+ cells expressed very large amounts of Il9 transcript (>105 fold), compared to naive CD4+ T cells (Figure 2E).
0.94 Il9, Il13, and Mcpt6, while maintaining Gata2 gene expression after culture with SCF, IL-4, TGF-beta, and IL-33 (Figure S2G and data not shown).
0.92 IL-9 and IL-13, with considerably less IL-5 and no IFN-gamma (Figure 2F).
0.91 IL-9, the key cytokine for the proliferation, maturation, and activation of MCs; vi) Distinct from other IL-4 and IL-13-producing non-lymphoid cells (MCs, basophils, and eosinophils), which develop normally in STAT6 or IL-4Ralpha-deficient mice, inasmuch as MMC9 development requires the IL-4 and STAT6 signals; and vii) IL-9 and L-9R signals are important to establish pulmonary and intestinal mastocytosis, but is dispensable for MMC9 induction.
0.88 IL-9 (~0.05 pg/mL per cell) as well as IL-4, IL-5, and IL-13 (Figure 2A and 2B and data not shown).
11686869 0.98 IL-9 and IL-13 have been shown to mediate AHR in the allergic lung, and blockage of either cytokine by using neutralizing antibody or soluble receptor is sufficient to attenuate AHR in selective animal models.
0.98 IL-13 or IL-9 showed increased allergic inflammation, AHR, and mucous cell metaplasia, and induction of genes encoding lung chemokines, proteases, adhesion molecules, and mucins.
0.98 IL-9-deficient mice in the pulmonary granulomatous model, IL-13-deficient mice developed a global downregulation of the TH2 response with smaller granulomas around S. mansoni eggs, a reduction in lung eosinophilia, and reduced IL-4, IL-5, and IL-9 productions from cultured lymph nodes, indicating a role for IL-13 as a general enhancing factor on TH2 response.
0.97 IL-9, but not IL-5 or IL-13, might account for most of the mucin-stimulatory activity of lung fluids in allergic airway disease.
0.95 IL-9, IL-13, and numerous growth factors and receptors implicated in allergic inflammation.
0.95 IL-9, and IL-13 that are thought to alter gene regulation or function, and are potentially associated with atopy and asthma.
0.95 IL-9, mice treated with IL-13 had a greater cellular influx and inflammation-related gene upregulation at lower IL-13 doses and after fewer intratracheal instillations.
0.94 IL-9 as a critical mediator of allergic asthma, comparing these data with similar studies on IL-4, IL-5, and IL-13.
0.63 IL-9-deficient mice expressed normal levels of IL-4, IL-5, and IL-13.
24249111 0.98 IL-9 signaling, most likely by promoting ILC2 accumulation and enhancing production of IL-5 and IL-13 by ILC2s, can influence the function of eosinophils and alternatively activated macrophages that contribute to damage repair mechanisms in the lung.
0.98 IL-9, IL-13, and IL-5, ILC2s produce the epidermal growth factor family member amphiregulin and thereby promote the regeneration of bronchiolar epithelium after influenza infection in Rag1-/- mice.
0.98 IL-9 promotes IL-5 and IL-13 production (at that time attributed mainly to Th2 cells) in the lung (Temann, Ray, and Flavell, 2002) and gut-associated lymphoid tissue.
0.98 IL-9, IL-13, and potentially other mediators that may enhance damage repair by either directly acting on tissue-resident cells or by changing the abundance and/or activation status of other immune cells.
0.97 IL-9 production in ILCs was transient but important for the maintenance of IL-5 and IL-13 in ILCs.
0.97 IL-13 production in Il9 transgenic mice were not abrogated, but in contrast even enhanced on a T cell- and B cell-deficient background, strongly suggesting that an innate cell type and not Th2 cells is one of the major targets of IL-9.
0.96 IL-9 resulted in strongly increased production of IL-5 and IL-13 in WT but not in Il9r-deficient ILC2s (Fig. 10 A).
0.94 IL-13 expression in ILC2s is regulated by IL-9, albeit the underlying mechanism and the functional importance of ILC2-derived IL-9 was not addressed.
0.82 Il9 transgenic mice is abolished if these mice are crossed to an IL-13-deficient background.
29339496 0.98 IL-9, and IL-13.
0.97 IL-13 dual-reporter mice to show that naive CD4+ T cells cultured in the presence of IL-4 and thymic stromal lymphopoietin (TSLP) generate a population of IL-4negIL-13pos Th2 cells that develop from IL-4neg precursors and express the Th2 effector cytokines IL-5 and IL-9.
0.96 IL-13, IL-5, and IL-9.
0.95 IL-13-SP Th2 cells originated from IL-4-negative precursors and coexpressed transcripts for the Th2 cytokines IL-5 and IL-9.
0.95 IL-13-DsRed single-positive (IL-13DR SP) CD4+ T cells that also expressed Il5 and Il9 transcripts and originated from IL-4-AmCyan (IL-4AC)-negative T cell precursors in vitro.
0.95 IL-13+ cells generated in Th2+TSLP cultures are heterogeneous and include subsets that also produce IL-9 and/or IL-5.
0.94 Il9, and Il13 transcripts, but not Il10 or Ifng.
0.86 Il13, Il5, and Il9 transcripts compared with control, whereas Il10 and Ifng transcripts were similar.
0.74 Il13, Il5, and Il9 transcripts; similar Il10 and Ifng; and lower Il4 compared with T cells cultured without TSLP.
29872093 0.98 IL-13, accumulating evidence demonstrated a central role for IL-9 in mediating immunity to intestinal helminth parasites in the mouse system.
0.98 IL-13 and the efficient expulsion of the helminth S. ratti from the intestine but that IL-9 is dispensable for the establishment of protective immune memory.
0.98 IL-9 functions as a central autocrine survival factor for ILC2 that initiate and amplify the adaptive type 2 immune response during helminth infection and allergic inflammation via production of IL-13 and IL-5, as demonstrated in C57BL/6 mice.
0.97 IL-9 functioned as a non redundant mast cell activating effector cytokine, induced intestinal IL-13 transcription and promoted parasite expulsion from the intestine irrespective of the genetic background of the host.
0.95 IL-9-dependent induction of IL-13 in hematopoietic cells, such as mast cells or ILC2, as shown for IL-9-induced asthma, is still possible.
0.95 IL-13) or statistically significant (IL-4 and IL-9).
0.88 IL-13 did not change intestinal parasite burden whereas neutralisation of IL-9 increased parasite burden, suggesting that IL-13-mediated effects are not as important for intestinal immunity to S. ratti as IL-9-mediated effects.
0.82 IL-13, IL-4, IL-3 and IL-9 by MLN but still displayed elevated parasite burden in the intestine, argues against that.
0.55 IL-9 responsive source of IL-13 and ILC2 have been involved in immunity to S. venezuelensis, we quantified ILC in the Lamina Propria and Peyer's Patches of WT and IL-9R-/- BALB/c mice.
29540816 0.98 IL-13 and IL-9, are known to stimulate effector mechanisms that drive worm expulsion.
0.97 IL-13 and IL-9 produced by naive lymphocytes in response to stimulation with these fractions, suggesting that these fractions contain parasite-specific antigens that drive Th2 cytokine release during acute infection.
0.97 IL-13 and IL-9 in response to stimulation with fractions 17 to 23, again demonstrating that these fractions contain parasite-specific antigens capable of driving Th2 cytokine production during acute infection.
0.95 IL-13), and inducing intestinal hypercontractility (IL-9).
0.91 IL-13 (and to a lesser extent IL-9) production by CD4+ T cells, we reasoned that a screening method involving the identification of IL-13 inducing T. muris antigens could identify potent vaccine candidates.
0.85 IL-13 (and IL-9) secretion by infection-primed MLN lymphocytes.
0.79 IL-13 and IL-9 production in order to identify immunogenic candidates.
0.75 IL-13 and IL-9 cytokine production by infection-primed lymphocytes was highest in response to stimulation with sub-groups 3 and 4 (Fig. 1d and e), whereas the highest anti-parasite antibody levels were measured in response to sub-group 2 (Fig. 1f).
23727894 0.98 IL-9 also promotes IL-13 expression in airway epithelial cells, which further amplifies the effect of IL-13.
0.98 IL-9 and IL-13 have been shown to be important regulators of lung inflammation, especially in acute allergic responses.
0.97 Il13 and Il9 mRNA than did their wild-type (CD45.1+) counterparts (Supplementary Fig. 10d).
0.96 Il13 and Il9 mRNA than did that from CIS-sufficient mice (Fig. 3d and Supplementary Fig. 8d).
0.93 IL-13 (refs.) and the TH9 cytokine, IL-9 (refs.).
0.89 IL-13, IL-9 is also associated with allergic asthma.
0.83 Il13 and Il9 mRNA than did that from Cisfl/fl mice (Fig. 4d).
20154671 0.98 IL-9 production and inhibits the production of classical TH2 cytokines, IL-4, interleukin 5 (IL-5), and interleukin 13 (IL-13).
0.97 IL-13 and IL-9 expression, this effect was completely absent in IL-17RA-deficient T cells (Fig. 4a).
0.92 IL-13 production in splenocytes from anti-IL-9 treated CD4-IL-17RB transgenic mice (Fig. 6d).
0.90 IL-9 production as well as IL-5 and IL-13 production (Fig. 2c).
0.76 IL-9 and marked reduction of IL-4, IL-5, and IL-13.
0.63 IL-9 expression, although it did not affect IL-5 and IL-13 expression.
22566857 0.98 IL-9, and IL-13.
0.98 IL-9 fate reporter mouse model established that besides the Th2-type cytokines IL-5, IL-6, and IL-13 ILC2 also produce IL-9 (Wilhelm et al.,).
0.98 IL-13 production in ILC, IL-9 is not permanently expressed but characterized by a very transient IL-2 dependent expression profile thus extending the portfolio of cytokines released by ILC.
0.98 IL-9 expression from ILC further enhancing/maintaining IL-5 and IL-13 expression thus possibly contributing to augmented worm expulsion.
0.97 IL-9 promotes expression of IL-5 and IL-13 from ILC and IL-2 induces IL-9, the lack of IL-2 from adaptive immune cells (or NKT cells), and the resulting loss of IL-9 expression is one possible explanation for reduced Th2-type cytokine expression in Rag-/- mice.
0.97 IL-9 to Rag-/- mice in the context of allergen challenge resulted likewise in increased levels of IL-5 and IL-13 (unpublished data).
26936133 0.98 IL-9, in addition to IL-4 and IL-13 (refs).
0.98 IL-9, IL-5 and IL-13 cytokines in response to stimuli compared to WT ILC2s (Fig. 9g).
0.98 IL-13 and IL-9, which can induce Th2 differentiation.
0.97 IL-9 also contributes to pathology in inflammatory bowel disease and autoimmune diseases, in addition to asthma models, where it was shown to induce mucus production, goblet cell metaplasia, expression of IL-13 and airway hypersensitivity.
0.95 IL-9-expressing infiltrating T cells were significantly reduced in Itk-/- mice, as seen for IL-4 and IL-13-expressing T cells (Fig. 8e).
0.75 IL-9+ILC2 and IL-13+ILC2 cells 2 weeks post-sensitization with papain (Fig. 9b).
29511181 0.98 interleukin (IL)-9 and IL-13, and are dependent on transcription factors GATA-binding protein 3 (GATA3) and retinoic acid receptor-related orphan receptor-alpha (ROR-alpha) for development and function.
0.97 IL-9 and IL-13 following sepsis, and demonstrated that both cytokines were markedly increased between 12 and 24 h after CLP (Fig. 4c).
0.97 IL-9 and IL-13 in plasma and bronchoalveolar lavage fluid (BALF) after sepsis as compared with those in WT mice (Fig. 4d).
0.97 IL-9 and IL-13 were decreased, and rmIL-33 could rescue the phenotype, highlighting a role for IL-33 in ILC2 expansion and activation.
0.91 IL-9, and IL-13 expression in the ILC2 increased in the lungs by flow cytometry.
0.89 IL-9 positive (IL-9+) ILC2 significantly increased by 24 h after CLP, and IL-13+ ILC2 transiently increased after CLP and reached a peak at 6 h (Fig. 4a, b).
19692641 0.98 IL-9 and IL-13 and a statistically significant reduction of TNF-alpha, IL-6 and IFN-gamma (Fig 5B).
0.98 IL-9 and IL-13, but also with a significant decrease in production of these pro-inflammatory cytokines from MLN cells (Fig 1B, Fig 5B and Fig 6B).
0.97 IL-9 and IL-13 and reductions in the pro-inflammatory cytokines TNF-alpha and IL-6, while IFN-gamma and IL-10 levels remained comparable to males in these mice (Fig 1B).
0.96 IL-9 and IL-13 production and a decrease in pro-inflammatory cytokines.
0.84 IL-9 and IL-13, and reduced pro-inflammatory cytokines (Fig 6B).
20847745 0.98 IL-9 was first linked to T helper 2 (TH2) cells, which express IL-4, IL-5 and IL-13, following the report that levels of IL-9 expression were high in the TH2-prone BALB/c mouse strain but low in the TH1-prone C57BL/6 mouse strain during infection with Leishmania major.
0.98 IL-9 can enhance mast cell expression of several cytokines, including IL-1beta, IL-5, IL-6, IL-9, IL-10 and IL-13 (REF.).
0.98 IL-9 contributes to disease by promoting mast cell expansion and production of IL-13, which in turn promotes the release of mucus that contributes to airway hyperresponsiveness.
0.96 IL-13, but not IFNgamma, by IL-9-producing NKT cells.
0.93 IL-13 are of particular interest, as the previously described direct effects of IL-9 in promoting eosinophilia and mucus production in the lung and the gut instead seem to be indirect effects mediated through the induction of these cytokines by IL-9 (REFS).
25175771 0.98 IL-9 and IL-13, in response to the cytokines, such as IL-25, IL-33 and thymic stromal lymphopoietin (TSLP), that are devived from epithelial cells and certain immune cells.
0.98 IL-9 might form a positive feedback loop that amplifies production of IL-5 and IL-13 by ILCs during allergic responses.
0.97 IL-9, IL-13 and GM-CSF protein.
0.97 IL-9 and IL-13 induce mast cell differentiation and maturation.
0.97 IL-9 to purified lung ILCs enhanced the production of IL-5, IL-6 and IL-13 by ILCs, and neutralization of IL-9 reduced the production of these cytokines in the lungs.
26891006 0.98 IL-9, and IL-13, and require the transcription factors RORalpha and Bcl11b for their development and maturation.
0.98 IL-9 produced by ILC2 cells promotes ILC2 survival by inducing upregulation of the anti-apoptotic protein, Bcl3, and inducing IL-5 and IL-13 production in an autocrine manner.
0.96 IL-13 but also IL-9.
0.96 IL-9 and IL-13.
0.96 IL-9 induces airway hypersensitivity and IL-13 causes airway hypersensitivity as well as activation of M2 macrophages.
29399438 0.98 IL-9, IL-13 and amphiregulin.
0.98 IL-9 and IL-13 as well as other tissue remodeling factors such as arginase 1 (Arg1) and amphiregulin (Areg).
0.98 IL-9, and IL-13 that support the development of immunity and inflammation at barrier surfaces.
0.97 IL-9 and IL-13, are known to assist in polarizing naive CD4+ T cells to TH2 cells as well as to promote other critical events.
0.97 IL-9 and IL-13, which promote many aspects of type 2 immunity that are described above and are comprehensively reviewed in several articles.
30617299 0.98 IL-9, and IL-13).
0.98 IL-9 and IL-13 production that generates goblet cell hypertrophy and mucus production.
0.97 IL-9, and IL-13.
0.97 IL-9 enhances the survival and/or proliferation of ILC2 as well as the production of IL-5 and IL-13 that together leads to an allergic immune environment.
0.96 Il-9, IL-13 and TGFb compared with ILC2 cells in media alone (Figure 8E).
31072011 0.98 IL-9 signaling on ILC2s is important for their expansion and production of IL-5, IL-13, and epidermal growth factor receptor (EGFR)-ligand amphiregulin in the lung.
0.98 IL-9 is upregulated in ILC2s in response to epithelial damage and signals in an autocrine manner to induce IL-5, IL-13, and amphiregulin.
0.97 IL-13 production in the lung is largely dependent on alarmin IL-33 and cytokine IL-9 during Strongyloides venezuelensis and N. brasiliensis infections .
0.97 IL-13, and small amounts of IL-4, ILC2s are also key producers of IL-9.
0.97 IL-9 induces mastocytosis, eosinophila, mast cell infiltration, and mucus production indirectly via IL-4, IL-5, and IL-13, and serves as a T cell and mast cell survival and growth factor.
22327077 0.98 IL-9, IL-13) that were initially thought to be of Th2 cell origin.
0.98 IL-9 by IL-9 mAB i.v. not only inhibited airway inflammation and hyperreactivity, but also suppressed IL-4, IL-5, and IL-13 in the BAL indicating that IL-9 controls the expression of Th2 cytokines and possesses higher asthmatogenic potency than other asthma-promoting cytokines.
0.97 IL-9 was found to be at least partially mediated by IL-13 that was produced from airway epithelial cells.
0.97 IL-13 was induced by IL-9 used IL-9 overexpressing mice, leading most likely to non-physiological and permanent high local concentrations of IL-9.
23053395 0.98 IL-9, IL-13) and decreased levels of Th1-associated cytokines (IFN-gamma, IL-12p40).
0.98 IL-9 and IL-13.
0.97 IL-9 and IL-13, cytokines associated with a Th2-type immune response, but can also cause increased gut pathology.
0.96 IL-9 but normal IL-13 production.
24876829 0.98 IL-9 is an autocrine factor necessary for amphiregulin, IL-5, and IL-13 production, as well as eosinophil recruitment.
0.98 IL-9 dependent on IL-2, and ILC2 cultured with IL-9 showed increased production of IL-5, IL-6, and IL-13.
0.97 IL-13 induces airway hyperresponsiveness, and along with IL-9, promotes mucus production.
0.65 IL-9 enhanced mast cell release of IL-6 and TNFalpha, while IL-13 had the opposite effect and suppressed mast cell release of IL-6 and TNFalpha.
29535264 0.98 Il9, and Il13 expression in CD4+ T cells; thus, its loss leads to increased production of TH2 cytokines.
0.96 IL-9, and IL-13.
0.88 IL-9, and IL-13.
0.84 Il13, and Il9 genes.
29773890 0.98 IL-9 -IL-13.
0.98 IL-13-overexpressing mice develop intestinal goblet cell hyperplasia and the administration of exogenous IL-25 or IL-9 induce goblet cell hyperplasia and increased mucin expression via IL-13 dependent pathways.
0.98 IL-13 when infected with the nematode Nippostrongylus brasiliensis, implying that IL-17, either directly or indirectly, through the intervention of IL-25 or IL-9, promotes a Th2 response.
0.97 IL-13 and IL-9 production and consequently modifies the physiological conditions suitable for the establishment of gastrointestinal nematodes through the stimulation of the hostile conditions described above.
22546005 0.98 p40) (789 %), IL-12(p70) (289 %), IL-13 (784 %), IL-15 (570 %), INF-gamma (253 %), TNF-alpha (626 %) and IL-10 (1,210 %), many of which participate in the activation of the antiviral innate immune response.
0.98 IL-9, IL-13, IL-15, IL-17 and IL-10, indicating that cytokines are physiologically present in the developing brain without the induction of an innate immune response.
0.95 IL-9, IL-13, IL-15, IL-17 and IL-10.
25746972 0.98 IL-9, but not IL-13, cytokine required for many aspects of allergic inflammation.
0.95 IL-9 or IL-13 diminished allergic inflammation.
0.77 IL-9 was required for Th9 cells to mediate mast cell accumulation, whereas IL-13 was not required.
26117252 0.98 IL-13, IL-9, and amphiregulin.
0.96 IL-9, IL-13 and GM-CSF.
0.93 IL-13 and IL-9, as well as certain growth factors, such as amphiregulin.
26371249 0.98 IL-9 and partially contributed to production of IL-13 and IL-5.
0.96 IL-13 and IL-5, ILC2s may also transiently produce IL-9 after encounter with IL-25.
0.95 IL-9, but not IL-13 mRNA, was also decreased in CCL17 KO mice.
27472835 0.98 IL-13, and IL-9 in db/db but not WT mice (Figure 2A-C).
0.98 IL-13 were reduced in anti-ST2 versus isotype antibody treated obese mice exposed to O3 and a similar trend was observed for IL-9 (Figure 3), indicating a requirement for IL-33 in the induction of these type 2 cytokines by O3.
0.95 IL-13 and IL-9, O3 also caused greater increases in BAL CXCL1, IL-6, IL-2, eotaxin (CCL11), CSF3, IL-1alpha, IL-10, IL-12 (p40), CXCL10, LIF, RANTES, CXCL9, and CCL4 in the same cohort of O3-exposed isotype-treated db/db versus WT mice (Figure 2D-P).
27492902 0.98 IL-9, Irf4, Il13 and the Th2-related transcription factor Gata3 (Fig. 1b-d), whereas the expression of other Th-related cytokines and transcription factors remained unchanged (Fig. 1c,d).
0.89 IL-9, Irf4, Il13 and Gata3 as compared with those primed by BMDCs (Fig. 2a-c), Th9 cells primed by alphaDectin-1-treated CurDCs expressed significantly lower levels of IL-9, Irf4, Il13 and Gata3 than those primed by CurDCs (Fig. 2a-c).
0.53 IL-9, Irf4 and Il13 expression in CurDC-induced Th9 cells as compared with the treatment of control IgG (Fig. 4c,d and Supplementary Fig. 7A,B); whereas the addition of alphaTNFSF15 did not affect IL-9 expression of BMDC-induced Th9 cells (Fig. 4c,d and Supplementary Fig. 7A,B).
27909880 0.98 IL-9 and some TH2 cytokines (IL-4, IL-5, and IL-13).
0.98 IL-9 transiently, which facilitated IL-5 and IL-13 production in an autocrine manner.
0.94 IL-9 (~2.0 pg/mL per cell) and other TH2 cytokines, including IL-4 and IL-13, in lesser amounts; iii) exhibiting a small innate helper cell-like morphology with few metachromatic granules in their scanty cytoplasm; iv) secreting MC proteases and histamine.
24586147 0.98 IL-9 in this setting was demonstrated to positively regulate IL-5 and IL-13 responses, likely ILC2-derived IL-5 and IL-13 as TH2 cell numbers were unchanged in IL-9R-deficient animals, promote ILC2 cell survival, drive lung tissue repair mechanisms, and promote eosinophil recruitment and alternative activation of macrophages.
0.87 IL-9 but not IL-13 production in mesenteric lymph nodes.
25201407 0.98 IL-13, IL-9 has also been shown to be induced by T. muris infection and to play an important role in protective immunity.
0.98 IL-9 and IL-13), regulatory (IL-10 and TGF-beta) and mucosal healing (IL-22) cytokines.
26965110 0.98 IL-9 production by ILC2s, resulting in increased IL-5 and IL-13.
0.96 IL-9 was also induced in response to chitin, resulting in an increased IL-5 and IL-13 production.
28196875 0.98 Il9 and Il13 are Th2-related cytokines.
0.96 Il9 and Il13 (Figure 4A and 4B).
28497800 0.98 IL-9 and IL-13 (which is regulated by IL-9 in asthma) were strongly diminished by IL-9 neutralization (Supplementary Fig. 6d,e).
0.97 IL-9 and IL-13 but less IFN-gamma (Fig. 5c-e), revealing that Irf1-/- Th9 cells retain their pro-allergic phenotype in vivo as compared to WT Th9 cells.
28739029 0.98 IL-9 was shown to induce mast cell to produce multiple other cytokines, including IL-5, IL-6, IL-9, IL-10 and IL-13, which mediate allergic inflammation.
0.98 IL-9 is required for ILC2 cell functions, as neutralization of IL-9 leads to reduced expression of IL-5 and IL-13 by ILC2 cells.
30650370 0.98 IL9 and IL13 expression (Figure S7C-E).
0.94 IL-9 and IL-13, but not IL-2 production (Figure 7D, S5B).
29176972 0.98 IL-9, IL-10, and IL-13, high type 2 anti-Leishmania antibody titers, and alternative activation of macrophages, which altogether promotes parasite survival and growth (Figure 2).
22783250 0.97 IL-9 in the lung induces an asthma-like phenotype in an IL-13-dependent manner (Temann et al.,) and blocking of IL-9 reduces airway hypersensitivity (Kung et al.,; Cheng et al.,).
0.97 IL-9 induces mucous production, goblet cell hyperplasia, and other features of airway remodeling (Townsend et al.,; Kearley et al.,), effects shared by IL-13 via goblet cell hyperplasia (Wynn,) and IL-5 via eosinophilia (Cho et al.,).
0.97 IL-9 in the lung (Tan et al.,), raising the possible involvement of an IL-9/IL-13 axis in airway hypersensitivity induced by innate lymphocytes.
0.97 IL-9, and IL-13 and the appearance of IL-9fm+ cells in bronchoalveolar lavage fluid, most of which are Lin-CD45+CD90+ cells.
0.96 IL-9/IL-13 axis in the lung.
0.95 IL-9, and IL-13 in the lung but administration of anti-IL-2 mAb reduced only IL-9 production.
0.93 IL-9, and IL-13 (Wilhelm et al.,).
0.90 IL-13 but not IL-4 or IL-9 by IL-9fm+ cells.
0.55 IL-9 producing cells were mostly Lin-CD90+ cells, which also produce IL-13.
26553024 0.97 IL-9, IL-12 (p70), IL-13, G-CSF, GM-CSF, MCP-1, MIP-1alpha, MIP-1beta and TNF-alpha.
0.97 p40)) and two structural hubs (IL-13 and MCP-1) were responsible for orchestrating the most significant changes within the network, thereby reinforcing the proposed concept of a signal integration role played by the latter two cytokines.
0.96 IL-9, IL-10, IL-12 (p40), IL-12 (p70), IL-13, eotaxin, G-CSF, IFN-gamma, KC, MCP-1, MIP-1alpha and RANTES to decrease on day 2 of lactation.
0.96 p40), IL-13 and MCP-1 may prove valuable in the exogenous manipulation of inflammatory networks.
0.94 p40), IL-13 and MCP-1 drive murine cytokine networks in vivo
0.93 p40) in those governing T cell and macrophage responses, IL-13 in the pathophysiology of ulcerative colitis, IFN-gamma, IL-12 (p40/p70) and MCP-1 in Erdheim-Chester disease and eotaxin, IFN-gamma, MIP-1alpha and MIP-1beta in asthma.
0.93 p40) and IL-13 perturbation which, independently, are both known to increase IFN-gamma concentration.
0.75 IL-13 and/or IL-12 (p40)
0.51 p40), IL-13 and monocyte chemoattractant protein (MCP)-1 were the primary drivers of network behavior.
22277204 0.97 IL-9 and IL-13 released from antigen-stimulated lymphocytes isolated from lung draining lymph nodes of allergic mice (Fig 4, H and I).
0.95 IL-13 and IL-9 levels in cultures from mice transferred with TH9 cells, compared with those treated with HDM alone (Fig 3, H and I).
0.94 IL-9+IL-13- cells express the transcription factor PU.1 (42.9 +- 3.9), but this was not true for all TH9 cells (Fig 1, G).
0.93 IL-9 but not IL-13 or IL-10, and were observed in the lungs following intraperitonial injection (see Fig E3, A and B, in this article's Online Repository at www.jacionline.org).
0.91 IL-9+IL-13-IFN-gamma-IL-17- cells were only rarely observed in lungs from naive mice; however, inhalation of the environmental allergen HDM led to the early in vivo differentiation of TH9 cells (Fig 1, D; see Fig E1, A, in this article's Online Repository at www.jacionline.org for flow plots).
0.90 IL-9-blocking antibody, which resulted in the abrogation of mast cell recruitment with a concomitant reduction in airway remodeling, partial resolution of AHR, but no effect on classical TH2 pathological features such as IL-13, IL-5, and eosinophilia.
0.89 IL-9+IL-13-IFN-gamma-, in allergic donors than in nonallergic donors (Fig 1, A).
23174661 0.97 IL-9 can affect IL-13 and IL-10 production by T cells, the effect of PD-L2 on various cells can also contribute to the reduction in IL-13, IL-10, and TGF-beta levels.
0.96 IL-9, IL-10, IL-17a, and IL-13 significantly increased (Fig 3, B).
0.93 IL-13-, and IL-17a-producing CD4+ T cells were still detected both in the lungs and LNs of A fumigatus-sensitized mice, a significant population of IL-9-producing CD4+ T cells started to appear in the lungs (Fig 1, B) but not in the LNs (see Fig E1, B).
0.93 IL-9, IL-10, IL-13, and IL-17 were similar between WT and PD-L2-/- mice, whereas the intensity of the second peaks were enhanced in the lungs of PD-L2-/- mice.
0.92 IL-13, and IL-10 cytokines but not IL-9-producing CD4+ T cells both in the lungs and LNs of A fumigatus-sensitized mice (Fig 1, B, and see Fig E1, B).
0.92 IL-9, IL-13, IL-10, IL-4, IL-1alpha, and IL-17a were observed (Fig 5, B).
10510085 0.97 IL-9, and IL-13) than males (compare Fig. 8 with Table ) and elevated IgG1 responses during infection (data not shown).
0.95 IL-9, or IL-13 after in vitro restimulation with ES Ag (Table ), suggesting again that TNF-alpha may potentiate the effects of Th2 cytokines (in this case IL-13) rather than enhance their production.
0.91 IL-9, and IL-13 and promote mastocytosis, eosinophilia, and the production of IgE and IgG1 (for reviews, see references 1 2 3).
0.91 IL-9, and IL-13 at day 18 p.i.
0.81 IL-9 and IL-13 production was lower in anti-TNF-alpha treated mice than in the control Ig group (primarily as a result of the variability observed in this group; Fig. 8b and Fig. c).
27574500 0.97 IL-13, and IL-9 with IL-4.
0.97 IL-13, and IL-9.
0.91 IL-13 and IL-9 when stimulated with IL-33/SCF/IL-3 and release comparable amounts of histamine and MCP-1 as bone marrow-derived mast cells on ex-vivo IgE cross-linking.
24416647 0.97 IL-9, and IL-13) by IL-4 in a STAT6-dependent manner (canonical differentiation).
0.91 IL-9, but very little IL-4, IL-5, and IL-13.
27589682 0.97 IL-13, the TH9-associated cytokines IL-9, IL-10, and IL-21 are increased in various diseases.
0.97 IL-9, and IL-13), eosinophil maturation (IL-5 and GM-CSF), basophil infiltration (IL-4), and the initiation of mucus metaplasia (IL-13).
29122948 0.97 IL-13 and IL-5 production, miR-17~92 surprisingly reduced ILC2 expression of Il9, Il6, and Csf2 (GM-CSF).
0.94 Il13, as 17~92Delta/Delta ILC2s expressed higher levels of Il6, Csf2 (which encodes GM-CSF), and Il9 (Fig. 6 D).
31905768 0.97 IL-9 had potential to produce IL-5, IL-6, IL-13 and TNF-alpha upon IgE-mediated antigen stimulation.
0.97 IL-13 in BMMCs, whereas little or no induction of cytokine genes were observed in MCs/IL-9, raising a possibility that mast-cell-derived inflammatory cytokines should function at a very early stage of inflammation.
12045241 0.97 IL-9, IL-10, and IL-13) and Th2 cells are obligatory for the development and expression of disease.
28187441 0.97 IL-9, IL-13, and IL-17.
32148441 0.97 IL-9 KO significantly increased IL-1beta, IL-6, IL-17, TNF-alpha, IFN-gamma, and MCP-1 mRNA levels, whereas it reduced IL-4, IL-10, and IL-13 mRNA expression in Ang II-treated mice (Figure 4(b)).
23376058 0.96 IL-9 and IL-13 were only detected in the respective Th9 and Th2 cell cultures in the presence of TSLP (Fig. 1D).
0.96 IL-9-induced airway inflammation was dependent on IL-13, blocking IL-13 in Th9 cell recipient mice reduced airway inflammation and Th2 cytokines, but had little effect on IL-9 protein and gene expression in the lung (Fig. 5A-C).
0.95 IL-9+ population, Il9 expression and IL-9 production in Th9 cell cultures, and the IL-13+ population, Il13 expression and IL-13 protein production in Th2 cell cultures (Fig. 2A-C).
0.93 IL-13 in BALF (Fig. 4E), we next examined whether TSLP enhanced airway inflammation by promoting Th2 cytokine or IL-9 expression.
0.92 IL-13 and IL-9 in BAL from recipients of Th2 or Th9 cells, compared with OVA challenged mice.
0.84 IL-9+ cells than IL-13+ cells, and TSLP attenuated the loss of cytokine expression observed between transfer and harvest (Fig. 4D).
0.84 IL-13 in Th2 cells and IL-9 in Th9 cells, than in mice receiving the reciprocal cells (Fig. 4E).
0.70 IL-13, low IL-9) or Th9 cells (high IL-9, low IL-13) (Fig. 4A and B).
28898280 0.96 IL-9 and IL-13 production by mesenteric lymph node cells of T. spiralis-infected mice (Fig 2A).
0.96 IL-13, as well as Th9 cytokine, IL-9 (Fig 2C).
0.95 IL-9 and IL-13, stimulation with IL-25 significantly enhanced the secretion of IL-9 and IL-13 in the enriched ILC2s from isotype mAb-treated mice but not CD4 mAb-treated mice (Fig 3E).
0.95 IL-9, and IL-13.
0.94 IL-13 and moderate IL-9 but little IL-4 and IFN-gamma production; whereas, T. spiralis antigens triggered primarily IL-4, IL-5 and IL-9, but little IL-13 and IFN-gamma production by mesenteric lymph node cells from T. spiralis-infected mice (Fig 2A).
0.94 IL-9 and IL-13 cytokines, but larger amounts of IFN-gamma than those from infected wild type mice (Fig 4E).
0.93 IL-9 and IL-13 production was less and antigen-specific Th2 and Th9 responses in mesenteric lymph nodes of CD4 mAb-treated mice at day 7 postinfection were significantly fewer than those of isotype mAb-treated mice, indicating that despite ILC2s remaining intact after depleting CD4+ T cells, these cells responded poorly to IL-25 stimulation (Fig 3D).
11781365 0.96 IL-9, and IL-13 cooperate to promote the development of AHR, however only IL-13 can compensate for a lack in IL-4 or IL-9.
0.96 IL-9 and IL-13 in regulating mucus cell hyperplasia are likely to be interrelated.
0.96 IL-9 may be involved in eosinophil recruitment by regulating chemokines such as eotaxin, IL-9 expression is not obligatory and other Th2 cytokines such as IL-4 or IL-13 can compensate for IL-9 deficiency.
0.91 IL-9 contributes to mucus production, but IL-13 is probably able to compensate for a deficiency in IL-9.
0.61 IL-9 is dominant, but IL-13 can compensate after multiple challenges.
16129701 0.96 IL-9, and IL-13 (Fig. 1 C).
0.95 IL-9, and IL-13.
0.95 IL-9, and IL-13 (Fig. 1 C).
0.94 IL-9, and IL-13.
0.93 IL-9 increased in mice injected with IL-2 and IL-18 and peaked at d 7; IL-13 was persistently elevated even beyond d 7.
29140165 0.96 IL-9, IL-3 and IL-13 (Fig. 3B).
0.94 IL-9 and IL-13 (Fig. 4A).
0.88 IL-9, IL-3 and IL-13.
25088770 0.96 IL-9, and IL-13, but little IFN-gamma or IL-17A, as compared to controls lacking peptide (Figure 5A; Figure S6A).
31284537 0.96 IL-9, IL-13, or IL-17, to activate eosinophils, basophil mast cells, or goblet cells.
21167580 0.95 IL-13, IL-9 and IL-10 (Fig. 6A-F) were all significantly increased in F709 mice gavaged with OVA and CT in comparison with respective controls.
0.78 IL-13, IL-5, IL-9, IL-33 and IFN-gamma transcripts in Y709 mice exposed to OVA and CT revealed no statistically significant increases in expression of any of these cytokines.
25458968 0.95 IL-13, as well as IL-9 and IL-10.
0.95 IL-13, whereas TGF-beta and IL-4 induce PU.1 expression which causes differentiation into the Th9 subset leading to the production of IL-9.
29867972 0.95 IL-9 overexpression further enhanced the production of Th2 cytokines such as IL-4, IL-5, and IL-13.
0.95 IL-13, and IL-9, hence it is needful to define and identify the predominant cytokine signature and subtype that is inducing the disease.
30761137 0.95 IL-9 may promote IL-13-mediated lung inflammation and mucus production, we found no difference in the frequency of lung-infiltrated IL-13-expressing Th2 cells in IL-9-treated mice, suggesting that other cells may have mediated the inflammatory process.
0.85 IL-9 treatment has no impact on IL-9+, IL-13+, and FOXP3+ CD4+ T cells in the lungs of butyrate-treated OVA-challenged mice.
28090087 0.95 IL-13 on exposure to IL-33 (ref.), an effect potentiated by IL-25 and thymic stromal lymphopoietin (TSLP), and IL-9 on the exposure to IL-2 (ref.).
21674475 0.94 IL-13 is required for IL-9.
23814672 0.92 IL-13 were decreased in BALF after exposure to anti-IL-9 Ab, which does not agree with our results.
0.91 IL-13 in addition to IL-9, and Th17 cells produce interferon (IFN)-gamma, IL-17, and IL-9.
23405898 0.92 IL-9 transgenic models, inflammation depends on IL-13.
20111717 0.89 IL-9, IL-10, IL-13, CCL17, CCL22, CD39 and CD73; IL-10 and IL-13 induce arginase 1 expression by MDSCs; CCL17 and CCL22 attract the migration of Treg cells; CD39 and CD73 enhance suppressor function of Treg cells; IL-9 produced by Treg cells maintains the survival of mast cells; MDSCs release active MMP9, through which soluble SCF is generated, thus further facilitating the migration and activation of mast cells.
22503540 0.89 IL-9 but comparable amounts of IL-10, IL-13, IL-17, and IFN-gamma compared to control Th9 and Th17 cells as measured by bead-based Luminex assay (Figure 1B) and by intracellular cytokine staining (Figure 1C).
30717817 0.89 Il9 (Fig. 3c), Il5 and Il13 (Fig. 3d) than mice transfused with Th9 cells or PBS control.
25099390 0.88 IL-9 production by ILCs depended on IL-2 and was rapidly lost in favor of IL-13 and IL-5.
24516385 0.86 IL-9 but not neutralization of IL-13 or depletion of granulocytes reverted the parasite burden to high levels and delayed the mast cell degranulation to normal kinetics in Treg-depleted BALB/c mice.
0.60 IL-9 production, we neutralized IL-9 and, as a control Th2 cytokine, IL-13 during Treg depletion in S. ratti-infected BALB/c DEREG mice (Figure 7A).
18997793 0.81 IL-13 and very low levels of IL-9.
19601851 0.74 IL-9 IL-10, IL-11, IL-13, and IL-19 to be anti-inflammatory interleukins (Table 1).
25360134 0.60 IL-9 producing CD4+ T-cells in vivo was not assessed in this study and the CD4dnTGFbRII mice had a decreased IL-4 response but normal IL-13 response to Trichuris, indicating possible defects other than the lack of IL-9, that could contribute to susceptibility.



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