Publication for Il5 and Il9

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression		 CoexViewer
mmu Il5 interleukin 5 16191 [link]
mmu Il9 interleukin 9 16198

Pubmed ID Priority Text
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 has a feedback effect on ILC, resulting in increased production of IL-5 and IL-13.
0.98 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-5, IL-6 and 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-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).
0.97 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-5 in IL-9 transgenic mice reduced eosinophil recruitment, suggesting that IL-5 production in this spontaneous airway inflammation is also linked with IL-9.
0.96 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.
0.96 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.
0.95 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).
0.95 IL-5 and 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.
0.90 IL-9 but sustained IL-5 and IL-13 production in ILCs
0.85 IL-5, IL-6 and 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.
31511826 0.98 IL-5, IL-9, IL-10, and IL-13).
0.97 IL-5, IL-9, IL-10, and IL-13 expression in CD4+ T cells.
0.97 IL-5, 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-5 and IL-9 mRNA expression.
0.97 IL-5, IL-9, IL-10, IL-13, and IFN-gamma in T cells.
0.97 IL-5, IL-10, IL-13, IL-9, and IFN-gamma cytokine production in T cells and enhance CD4+ T cell proliferation upon polyclonal stimulation.
0.96 IL-5, IL-9, IL-10, and IL-13 were observed to be increased compared to those of the control group.
0.96 IL-5, IL-9, IL-10, and IL-13 in T cells derived from KSRP+/+ mice during CAIA disease progression.
0.93 IL-5, 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)).
0.91 IL-5, IL-9, IL-10, and IL-13), we detected an increased production over time.
0.89 IL-5 and IL-9 in anti-CD3/CD28-stimulated splenic T cells isolated from PBS-treated KSRP-/- animals compared to the WT control.
0.87 IL-5, IL-9, IL-10, IL-13, or IFN-gamma mRNA and protein expression remains to be elucidated.
0.84 IL-5 and IL-13, as well as of IL-9 and IL-10 compared to control cells (Figures 1 and 2).
0.83 IL-5, IL-9, IL-10, IL-13, or IFN-gamma mRNA expression via direct or indirect mechanisms.
0.65 IL-5 and IL-9 3'-UTR (Figure 6).
32103032 0.98 IL-5, IL-9 or GM-CSF in response to IL-33.
0.98 IL-5, IL-6, IL-9, IL-13 and GM-CSF in response to IL-33 treatment.
0.98 IL-5, IL-6, 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.
0.98 IL-5, IL-6, IL-9, IL-13 and GM-CSF in response to IL-33 (Fig. 3A).
0.98 IL-5, IL-9 and GM-CSF in response to IL-33 stimulation was similar between wild type and MK2/3 knockout cells, indicating that these cytokines were regulated by p38 independently of MK2 and 3.
0.98 IL5, IL-6, IL-9, IL-13 and GM-CSF in IL-33 stimulated ILC2s.
0.97 IL-5, IL-6, 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-5, IL-9 and GM-CSF production were independent of MK2/3.
0.97 IL-5, IL-6, IL-9, IL-13 and GM-CSF (Fig. 4).
0.95 IL5, IL-6, IL-9, IL-13 and GM-CSF while MK2/3 and mTOR selectively drive IL-6 and IL-13 production.
0.94 IL-5, IL-9 and GM-CSF induction.
0.89 IL-5, IL-6, IL-9 and IL-13 following IL-33 stimulation.
0.88 IL-5, IL-9, and GM-CSF induction.
0.86 IL-5, IL-6, IL-9, IL-13 and GM-CSF (Fig. 5B-F).
0.77 IL-5, IL-6, 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).
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-5 production, suggesting that IL-9 from nearby ILC2s can induce cytokine production in neighboring cells (Figure 4f).
0.98 IL-9 requires IRF4 and acts in an autocrine manner to optimize IL-5 and IL-13 production.
0.98 Il5 and 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.
0.97 IL-9 rapidly generates IL-5, IL-13 and subsequent conducting airway proteins that drive tissue defense and repair.
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).
0.94 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).
0.85 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).
0.85 IL-9 also produced significantly less IL-5 or IL-13 in overnight ex vivo cultures (Figure 6b).
0.67 IL-5, 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).
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-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 Il5 and 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-5, 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.
0.95 IL-9 expression precedes IL-4, IL-5 and IL-13 during N. brasiliensis infection
0.89 IL-9 expression precedes IL-4, IL-5 and IL-13 in vivo
0.83 IL-9 expression also preceded that of IL-4, IL-5 and IL-13 (Figure S1).
31937554 0.98 IL-5, IL-9 and IL-13 are associated with eosinophil recruitment and survival in the lungs.
0.98 interleukin (IL)-5, IL-9 and IL-13, and eosinophil infiltration into the lungs, both of which augments lung inflammation after HS.
0.97 IL-5+ ILC2s, IL-9+ ILC2s and IL-13+ ILC2s in WT mice (figure 6A-C).
0.97 IL-5, 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-5, IL-9 and IL-13, mediates host protection through reducing tissue inflammation and enhancing tissue repair.
0.96 IL-5, IL-9 and IL-13 in plasma after HS as compared with WT mice (figure 6G).
0.94 IL-5+ ILC2s, IL-9+ ILC2s and IL-13+ ILC2s (figure 6A-C).
0.94 IL-5, IL-9 and IL-13 production in plasma at 24 hours post-HS (figure 6H).
0.89 IL-5+ ILC2s, 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).
0.83 IL-5+ ILC2s, IL-9+ ILC2s and IL-13+ ILC2s at 24 hours after HS (figure 6D-F).
0.82 IL-5 and 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).
11686869 0.98 IL-9 might therefore induce airway eosinophilia through the upregulation of IL-5 response and potentiating the IL-5-mediated maturation of eosinophil precursors.
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 has been shown to promote eosinophil maturation in synergy with IL-5.
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.
0.97 IL-5-induced maturation of eosinophils, IL-9 seems to act primarily by enhancing the activities of many other cytokines and factors.
0.97 IL-9 in the expulsion of the intestinal parasitic nematode Nippostrongylus brasiliensis, as previously suggested in the IL-9 transgenic mice, was completely compensated for by increased expression of IL-4 and IL-5.
0.95 IL-5, IL-9, IL-13, and numerous growth factors and receptors implicated in allergic inflammation.
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.
0.66 IL-9-deficient mice expressed normal levels of IL-4, IL-5, and IL-13.
28196875 0.98 Il5, Il9 and Il13 are Th2-related cytokines.
0.97 IL-5 and IL-9 depleted mice treated with L635 developed metaplasia normally after parietal cell loss.
0.96 Il5, Il9 and Il13 (Figure 4A and 4B).
0.95 IL-5 and IL-9 were significantly decreased in L635-treated IL33KO mice, we investigated the role of these Th2 cytokines in metaplasia induction in the stomach corpus.
0.93 IL-5 or IL-9 depleted mice had significant infiltration of F4/80-positive macrophages, most of which were co-positive for CD163 similar to non-specific IgG L635-treated mice.
0.92 IL-5 and anti-IL-9-treated mice had similar high levels of CD163-positive macrophages, and M2-macrophage polarization after L635 treatment was confirmed by high expression of Ym1 (Figure 5E and Supplemental Figure 3).
0.89 IL-5 or IL-9 depleted L635-treated mice had significant loss of Mis1-positive cells similar to non-specific IgG L635-treated mice.
0.88 IL-5 or IL-9 depleted mice have a significant percent of proliferating SPEM cells similar to non-specific IgG L635-treated mice.
0.77 IL-5 or IL-9 depleted L635-treated mice have a significant percent of SPEM cells similar to non-specific IgG L635-treated mice.
29339496 0.98 IL-5, IL-9, and IL-13.
0.96 IL-5 and IL-9.
0.96 IL-5, and IL-9.
0.95 IL-9 and/or IL-5.
0.94 Il5 and Il9 transcripts and originated from IL-4-AmCyan (IL-4AC)-negative T cell precursors in vitro.
0.94 Il5, Il9, and Il13 transcripts, but not Il10 or Ifng.
0.87 Il5, and Il9 transcripts compared with control, whereas Il10 and Ifng transcripts were similar.
0.74 Il5, and Il9 transcripts; similar Il10 and Ifng; and lower Il4 compared with T cells cultured without TSLP.
0.69 IL-9+ and IL-5+ cells also expressed 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-5, 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.
0.96 IL-9 production in ILCs was transient but important for the maintenance of IL-5 and IL-13 in ILCs.
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).
0.93 IL-5 and 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.
15823208 0.98 IL-9 prolongs eosinophil survival, as well as IL-5 mediated differentiation and maturation, suggests that IL-9 may potentiate eosinophil function in vivo.
0.97 IL-9 has shown a capacity to act on hematopoietic progenitors to enhance eosinophil development when added to CD34+ cells cultured with a mixture of IL-3 and IL-5.
0.94 IL-9 has a subordinate role compared to IL-5 in eosinophilopoiesis.
0.71 IL-5 was able to reduce eosinophil numbers in all tissue compartments, as well as BrdU+ eosinophils and CD34+ progenitor cells, and in all instances to a greater extent than anti-IL-9.
0.64 IL-9 in allergen-induced airway eosinophilia seems to be much smaller than that of IL-5, since the treatment with the single dose of the anti-IL-5 antibody (50 mug) significantly inhibited bone marrow, blood and airway eosinophilia, but the higher dose of anti-IL-9 (100 mug) was much less effective.
0.63 IL-9 antibody affects the allergic inflammation in a mouse model of airway eosinophilic inflammation and compared any such effect with the results of anti-IL-5 antibody treatment.
19592658 0.98 Il9, while having no effects on IL-5 or IL-13.
0.98 IL-9 is a pleiotropic cytokine involved in the pathologic and physiologic evolution of asthma by recruiting eosinophils and lymphocytes to the lung, inducing mucus hypersecretion, mast cells hyperplasia in concert with IL-4, IL-5 and IL-13, while IL-10 is a suppressive cytokine that may modulate many of these processes.
0.97 IL-5, IL-9, IL-13, and other cytokines including the anti-inflammatory cytokine IL-10.
0.97 IL-5, but a decrease in Il9 mRNA (Fig. 2C).
0.96 IL-5 or IL-13 production and decreased Il9 transcription.
0.91 IL-9 and having little effect on IL-5 or IL-13.
26891006 0.98 IL-5, 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.
0.97 IL-5, IL-9 and IL-13.
0.96 IL-5 and IL-13 but also IL-9.
0.96 IL-5 induces eosinophilic inflammation, IL-9 induces airway hypersensitivity and IL-13 causes airway hypersensitivity as well as activation of M2 macrophages.
29399438 0.98 IL-5, IL-9, IL-13 and amphiregulin.
0.98 IL-5, IL-9 and IL-13 as well as other tissue remodeling factors such as arginase 1 (Arg1) and amphiregulin (Areg).
0.98 IL-5, IL-9, and IL-13 that support the development of immunity and inflammation at barrier surfaces.
0.97 IL-5, 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-5, IL-9 and IL-13, which promote many aspects of type 2 immunity that are described above and are comprehensively reviewed in several articles.
20847745 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.).
0.97 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.
0.96 IL-5 and IL-13, but not IFNgamma, by IL-9-producing NKT cells.
0.94 IL-5 and 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).
24508458 0.98 IL-5, IL-9, and IL-13 by Cblb-/- T cells supports the notion that Cbl-b may inhibit Th2 and Th9 cytokine production.
0.98 IL-5, IL-13, and IL-9 in BAL fluid compared with WT mice, which closely correlated with serum immunoglobulin E (IgE) production (Figure 2D).
0.96 IL-5, IL-9, and IL-13 was significantly higher in Cblb-/- T cells than in WT T cells (Figure 1A).
0.92 IL-5, IL-9, and IL-13 in the BAL fluid, and IgE in the serum, than those that received naive WT CD4+ T cells (Figure 2F).
25175771 0.98 IL-5, 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-5, IL-9, IL-13 and GM-CSF protein.
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.
31072011 0.98 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.
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-5, IL-13, and small amounts of IL-4, ILC2s are also key producers of IL-9.
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-5 production stimulates eosinophil activation and survival, whereas ILC2 IL-13 induces airway hyperresponsiveness, and along with IL-9, promotes mucus production.
26117252 0.98 IL-5, IL-13, IL-9, and amphiregulin.
0.97 IL-5, IL-9, IL-13 and GM-CSF.
0.93 IL-5, IL-13 and IL-9, as well as certain growth factors, such as amphiregulin.
27421480 0.98 IL-5, IL-6, IL-9, IL-13 and GM-CSF.
0.96 IL-5, IL-6, IL-9, IL-13 and GM-CSF.
0.91 IL-5, IL-13, IL-6, IL-9 and GM-CSF are unlikely to be responsible for this, although we cannot rule out the possibility that these cytokines may work additively or redundantly to promote IgG1 production.
27472835 0.98 IL-5, IL-13, and IL-9 in db/db but not WT mice (Figure 2A-C).
0.98 IL-5 and 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-5, 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).
26119026 0.98 IL-5, IL-9 and IL-13, and are resident in the airways, where they orchestrate type-2 immunity.
0.93 IL-5 (figure 5A), eotaxin-2, IL-4, IL-9, IL-10, IL-13, IP-10, MCP-1, TNF-alpha and TARC, but not IL-17, IL-23, IL-27, IL-28beta, INF-gamma and RANTES (table S1).
26371249 0.98 IL-9 and partially contributed to production of IL-13 and IL-5.
0.96 IL-5, ILC2s may also transiently produce IL-9 after encounter with IL-25.
26965110 0.98 IL-9 production by ILC2s, resulting in increased IL-5 and IL-13.
0.95 IL-9 was also induced in response to chitin, resulting in an increased IL-5 and IL-13 production.
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.
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.
30893794 0.98 IL-5, IL-9, and IL-13.
0.98 Il5, Il9, Il13, Csf2 encoding GM-CSF, and Areg encoding amphiregulin upon IL-33 stimulation is all downregulated in Cbfbeta-deficient ILC2s.
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.
30283458 0.98 IL-5, IL-13, and IL-9.
20154671 0.97 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-9 in CD4-IL-17RB transgenic T cells; TGF-beta blockade resulted in a reduction in IL-9 production but no change in IL-5 expression (Fig. 5a).
0.96 IL-5-producing TH2 cells appear distinct from IL-9-secreting T cells as assessed by intracellular cytokine staining (Fig. 1g) or IL-9 mRNA expression (Fig. 1h).
0.90 IL-5 and IL-13 production in splenocytes from anti-IL-9 treated CD4-IL-17RB transgenic mice (Fig. 6d).
0.89 IL-9 production as well as IL-5 and IL-13 production (Fig. 2c).
0.75 IL-9 and marked reduction of IL-4, IL-5, and IL-13.
0.58 IL-9 expression, although it did not affect IL-5 and IL-13 expression.
22783250 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-5, IL-9, and IL-13 and the appearance of IL-9fm+ cells in bronchoalveolar lavage fluid, most of which are Lin-CD45+CD90+ cells.
0.94 IL-5, IL-6, IL-9, and IL-13 in the lung but administration of anti-IL-2 mAb reduced only IL-9 production.
0.93 IL-5, IL-9, and IL-13 (Wilhelm et al.,).
0.92 IL-5 and IL-13 but not IL-4 or IL-9 by IL-9fm+ cells.
14970180 0.97 IL-5, IL-9, and IL-13) and GM-CSF are principally responsible for inducing bronchial asthma.
0.93 IL-5, IL-6, 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-5, IL-9, and IL-13 in response to IL-18 (Fig. 3 A).
0.89 IL-5, IL-6, IL-9, and IL-13 but not IFN-gamma, and Th1 cells produced IFN-gamma but not Th2 cytokines (Fig. 3 A).
23727894 0.97 Il5, Il13 and Il9 mRNA than did their wild-type (CD45.1+) counterparts (Supplementary Fig. 10d).
0.96 Il5, Il13 and Il9 mRNA than did that from CIS-sufficient mice (Fig. 3d and Supplementary Fig. 8d).
0.87 IL-5 and IL-13, IL-9 is also associated with allergic asthma.
0.82 Il5, Il13 and Il9 mRNA than did that from Cisfl/fl mice (Fig. 4d).
23814672 0.97 IL-9 blockade significantly attenuated the levels of IL-5, IL-9, IL-17, and IgE. These data indicate that the suppression of pulmonary inflammation by anti-IL-9 Ab is mediated through a decrease in multiple inflammatory mediators, including IL-17.
0.92 IL-5, and IL-13 in addition to IL-9, and Th17 cells produce interferon (IFN)-gamma, IL-17, and IL-9.
0.92 IL-5, and IL-13 were decreased in BALF after exposure to anti-IL-9 Ab, which does not agree with our results.
26410628 0.97 Il5 (>103 fold), 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).
0.89 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).
0.89 IL-9 and IL-13, with considerably less IL-5 and no IFN-gamma (Figure 2F).
11781365 0.97 IL-9 and evidence suggests that IL-9 may potentiate eosinophil function in vivo via interactions with IL-5.
0.97 IL-9 has been found to increase eosinophil survival, as well as IL-5-mediated differentiation and maturation.
22327077 0.97 IL-5, IL-9, IL-13) that were initially thought to be of Th2 cell origin.
0.97 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.
26878780 0.97 IL-5 secretion is consistent with Gurzell et al., who demonstrated that administration of DHA-enriched fish oil to Smad3-/- mice enhanced the frequency of B cells and increased secretion of IL-5, IL-9, and IL-13 in circulation.
0.95 IL-5 but not IL-9 or IL-13.
27574500 0.97 IL-5, IL-13, and IL-9 with IL-4.
0.97 IL-5, IL-13, and IL-9.
27589682 0.97 IL-5, and 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).
28615416 0.97 IL-5, IL-9 and IL-13) developed the same degree of protection as did recipients of IL-5 deficient CD4+ T cells; indicating a specific role for pathogenic IL-5 expressing CD4+ T cells in the spontaneous skin inflammation of the Il17ra-/- mice (Fig. 4G).
0.95 IL-5 deficient or IL-4/IL-5/IL-9/IL-13 deficient CD4+ T cells evoked significantly reduced skin barrier disruption (Fig. 4H).
29132961 0.97 IL9 and IL13 but not IL5 in bronchoalveolar lavage (BAL).
0.68 IL9+ and IL13+ but not IL5+ ILC2s.
31284537 0.97 IL-9 antibody inhibited the pulmonary infiltration of inflammatory cells and decreased the production of cytokines IL-5, IL-9, and IL-17 in murine asthma models.
0.96 IL-5, IL-9, IL-13, or IL-17, to activate eosinophils, basophil mast cells, or goblet cells.
12045241 0.97 IL-5, IL-9, IL-10, and IL-13) and Th2 cells are obligatory for the development and expression of disease.
23603794 0.97 IL-5, implicated in eosinophil recruitment, and IL-9 (ref.) which is prominent during helminth infections and has been linked to atopic disease.
25786692 0.97 IL-5, IL-6, IL-9, and GM-CSF fit these criteria and are upregulated by TL1A in both iTreg and Th9 conditions.
26936133 0.97 IL-9, IL-5 and IL-13 cytokines in response to stimuli compared to WT ILC2s (Fig. 9g).
28187441 0.97 IL-5, IL-9, IL-13, and IL-17.
29122948 0.97 IL-5 production, miR-17~92 surprisingly reduced ILC2 expression of Il9, Il6, and Csf2 (GM-CSF).
31905768 0.97 IL-9 had potential to produce IL-5, IL-6, IL-13 and TNF-alpha upon IgE-mediated antigen stimulation.
10224281 0.96 IL-9 Mediates an Increase in the Peritoneal B-1 Population in the Absence of IL-5.
0.95 IL-5 gene, overexpression of IL-9 resulted in a significant increase in the number of the B-1 population, and this expansion concerned mainly the B-1b population, as expected from the results described above (Fig. 8 A).
0.87 IL-9 in the absence of IL-5 ruled out the possibility that the effect of IL-9 is mediated by this cytokine.
0.81 IL-5 plays a role in B-1 cell development, it does not mediate the activity of IL-9 on this cell type.
0.56 IL-5 transgenic mice, in which expansion of the B-1 population is associated with high levels of autoantibodies, IL-9 did not stimulate the production of autoantibodies in vivo, and most of the expanded cells were found to belong to the B-1b subset (IgM+Mac-1+CD5-).
28898280 0.96 IL-5, IL-9 and IL-13 production by mesenteric lymph node cells of T. spiralis-infected mice (Fig 2A).
0.96 IL-5, IL-9, and IL-13.
0.94 IL-5 and 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-5, IL-9 and IL-13 cytokines, but larger amounts of IFN-gamma than those from infected wild type mice (Fig 4E).
0.93 IL-5, 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).
22546005 0.96 IL-5, IL-6, IL-12(p40), IL-12(p70), IFN-gamma, TNF-alpha and LIF), chemokines (LIX and MIP-2 ) and G-CSF were undetectable in brain homogenates despite the high sensitivity of the detection method, indicating that these factors are not present at detectable levels in the fetal brain under physiological conditions at this developmental stage.
0.70 IL-5, IL-6, IL-12(p40), IL-12(p70), IL-15, IL-17, IFN-gamma, TNF-alpha and LIF were not detected in fetal brain.
0.59 IL-5, IL-6, IL-12(p40), IL-12(p70), IL-15, IL-17, IFN-gamma, TNF-alpha and LIF were not detected in GD17 brain.
25230753 0.96 IL-9 or GM-CSF was detected in the supernatants from the purified preEos cultured with IL-5, suggesting that the IL-9 and GM-CSF detected in the supernatants from the LDBM cultures is produced and secreted by other bone marrow-derived cells in those cultures (Figure 3a).
0.83 IL-9 and GM-CSF, were detected after 5, 8 and 11 days of IL-5 stimulation of LDBM cells (Figure 3a).
0.77 IL-9, GM-CSF or IL-33 to the culture media for 2 days in the absence of IL-5 did not result in enhanced preEos maturation (as measured by upregulation of CCR3 on the surface of the Siglec-F+ preEos) compared to media alone (Figure 5c), but the frequency of preEos (Siglec-F+CCR3-) in the cultures increased with the addition of GM-CSF (Figure 5d).
29531070 0.96 Il9 revealed that both subsets were committed to Th9 differentiation but CD96low Th9 cells were characterized by higher IL-9 mRNA and protein levels, as well as IL-4 and IL-5 expression potential.
0.96 IL-9 production, CD96low Th9 cells were characterized by an increased IL-4 and IL-5 expression potential.
29535264 0.96 IL-5, IL-9, and IL-13.
0.89 IL-5, IL-9, and IL-13.
29867972 0.96 IL-9 overexpression further enhanced the production of Th2 cytokines such as IL-4, IL-5, and IL-13.
0.95 IL-5, IL-13, and IL-9, hence it is needful to define and identify the predominant cytokine signature and subtype that is inducing the disease.
30930900 0.96 IL-5 induction as one unwarranted side-effect of IL-2 immunocomplex treatment, however, it is important to note that stimulation of ILC2s with IL-2 or IL-2 immunocomplexes also induces other type 2 cytokines that may contribute to intestinal inflammation, including IL-9 and IL-13.
0.92 IL-5, IL-9, IL-13, and/or Ccl11 may enhance the effectiveness of IL-2 immunocomplex treatment during intestinal inflammation as well as other inflammatory disease settings.
21986312 0.96 IL-5 or SCF, IL-3, IL-9, GM-CSF, Epo, and Tpo, leading to differentiation exclusively into eosinophils.
29233972 0.96 IL-5 and IL-13 secretion and promotes IL-9 production.
21167580 0.95 IL-5, 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.
0.79 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.
23420878 0.95 IL-5 and IL-13; we have confirmed that VAT ILC2s spontaneously produce IL-5, IL-6, IL-13, and GM-CSF protein in culture, and can be induced in vitro with exogenous IL-33 or PMA stimulation to produce these cytokines, as well as IL-2 and IL-9.
0.94 IL-5, IL-6, IL-9, IL-13, and GM-CSF accumulated (Fig. 3 d), and these cytokines increased further with the addition of IL-2 or IL-7, similar to results reported by ILC2s from other tissues.
25458968 0.95 IL-5 and IL-13, as well as IL-9 and IL-10.
0.94 IL-5 and 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.
28090087 0.94 IL-5 and 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.).
26092469 0.93 IL-5, IL-9 and IL-13 were not required to mediate effects of ILC2 on Treg cells, suggesting that the downstream cellular targets of these cytokines, eosinophils and AAMs, are also not necessary.
0.86 IL-5, IL-4, IL-13, or IL-9; Treg cell expansion to IL-33 was normal in mice lacking these cytokines (Figure 3C, Figure S3D-E, data not shown).
9763610 0.92 IL-9-expressing mice seems to be a direct effect of IL-9, since mast cell hyperplasia in the airway epithelium has not been described in transgenic mice expressing other Th2 cytokines, IL-4, IL-5, or IL-6 selectively within their lungs.
0.91 IL-9, another Th2 cell-derived cytokine, in the lungs of our transgenic mice also resulted in an impressive inflammatory response that showed differences from that observed in IL-4 or IL-5 transgenic mice.
21674475 0.92 IL-5 and IL-13 is required for IL-9.
24879792 0.91 IL-9 production but did not affect the production of others cytokines, including IL-5, IL-17 and IFNgamma (Figure 3D).
30145844 0.91 IL-5, IL-9, and IL-13.TH2 cell-derived cytokines have pleotropic effects, which include stimulation of immunoglobulin E secretion by B cells (through IL-4), recruitment of eosinophils and mast cells (through IL-5 and IL-9, respectively), and increased mucus production, smooth muscle cell contractility, and vascular permeability (through IL-4, IL-9, and IL-13).
22277204 0.89 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.
25259859 0.89 IL-5, IL-9 and IL-13 gene activity and compromised Th2 responses, female mice reproduce successfully even during an allogeneic pregnancy.
30717817 0.89 Il9 (Fig. 3c), Il5 and Il13 (Fig. 3d) than mice transfused with Th9 cells or PBS control.
25099390 0.85 IL-9 production by ILCs depended on IL-2 and was rapidly lost in favor of IL-13 and IL-5.
26553024 0.84 IL-5, IL-9, IL-10, IL-12 (p40), IL-12 (p70), IL-17, IFN-gamma, G-CSF, GM-CSF, KC, MCP-1, MIP-1alpha, MIP-1beta, RANTES, P4 and PRL (Table 1 and Additional file 1).
18997793 0.81 IL-5, IL-13 and very low levels of IL-9.
15955840 0.80 IL-5, and IL-9, a small fraction of Lin- cells expressing an intermediate level of GFP appeared on day 3 (Fig. 1 C).
30914642 0.77 IL-9 production in Th9IL-4+IL-1beta cells (Fig. 1d, e), whereas Th9IL-4+IL-1beta or Th9IL-4+TGF-beta cells produced limited IL-4, IL-5, or IL-13 (Supplementary Figure 4).



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