Publication for TLR7 and TASL

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	TLR7	toll like receptor 7	51284			[link]
hsa	TASL	TLR adaptor interacting with endolysosomal SLC15A4	80231

Pubmed ID	Priority	Text
31695690	0.98	CXorf21 is more highly expressed in female compared to male cells and is involved in a sexually dimorphic response to TLR7 activation.
	0.98	CXorf21 co-localizes with lysosomal resident TLR7, and the CXorf21 SLE risk allele (rs887369) increases expression.
	0.98	TLR7-stimulated increase in CXorf21 mRNA (Figure 3E) and protein (Figure 3F) in the female monocytes after inhibition of CXorf21.
	0.98	CXorf21 decreased R837-activated TLR7 mRNA expression in primary female monocytes, suggesting a feedforward interaction between the two proteins (Figure 3G).
	0.98	CXorf21 is important for specific cytokine production via the TLR7 signaling pathway and this response is female biased.
	0.98	TLR7, CXorf21, SLC15A4 work together to regulate specific immune responses and lysosomal pH in female monocytes (Figures 6A,B).
	0.98	CXorf21, and TLR7, both putative risk genes in SLE that escape X-chromosome silencing, work together to drive the innate immune response in women, in a manner distinct from that found in men.
	0.98	CXorf21 in female immune cells that affects TLR7 signaling and interferon will be operative in autoimmune diseases in which the pathogenesis involves TLR7 signaling and an interferon signature.
	0.97	CXorf21 is required for SLC15A4-mediated TLR7 immune responses and the lysosomal pH gradient.
	0.97	CXorf21 in primary monocytes disrupts SLC15A4 function, and the regulation of Tlr7 expression.
	0.97	CXorf21 interacting partner, SLC15A4, regulates TLR7 downstream signaling led us to examine whether knockdown of CXorf21 would also abolish TLR7 immune response.
	0.97	CXorf21 is required for specific TLR7 downstream immune responses in female primary monocytes.
	0.96	TLR7 ligation increased CXorf21 protein expression and CXorf21 knockdown abrogated TLR7-driven increased IFNA1 mRNA expression, and reduced secretion of both TNF-alpha and IL-6 in healthy female monocytes.
	0.96	CXorf21 interacts with SLC15A4 to aid in modulation of NAPDH or H+ production, which may directly or indirectly affect the function of other endolysosomal proteins (i.e., TLR7, NOX2, V-ATPase pumps, other proton pumps, etc.) and their downstream responses (i.e., cytokine production, lysosomal pH).
	0.92	Tlr7 mRNA expression from female primary monocytes transfected with control (Con) or CXorf21-specific gRNA (CX21).
	0.92	CXorf21 decreases TLR7-stimulated IFN-alpha1, TNF-alpha, and IL-6.
	0.92	TLR7 is biallelically expressed in female and Klinefelter's syndrome male primary monocytes and B cells and our data confirmed that TLR7 was increased in male vs. female monocytes similar to CXorf21.
	0.91	CXorf21 and TLR7, which the present work shows interact functionally in innate immune responses, contribute to the pathogenesis of female-biased autoimmune disorders such as SLE and pSS, and may explain, in part, the propensity for women to have these diseases.
	0.82	CXorf21 and TLR7 in these immune response pathways provide a mechanism through which the X-chromosome gene dosage effect contributes to the disparate risk of SLE between the sexes.
	0.81	CXorf21 is involved in TLR7 signaling and IFN production and has a differential role between the sexes.
	0.75	CXorf21 protein and, moreover, is an integral piece into understanding the role this gene, in collaboration with other SLE putative risk genes, SLC14A4, X-linked TLR7, and potentially NCF1 (NOX2 subunit) contribute to the X-chromosome dose effect that explains the female bias in SLE and pSS.
	0.72	CXorf21 is still unknown, published data show that CXorf21 interacts with SLC15A4, and Slc15a4-deficient cells had decreased TLR7-stimulated immune response and increased lysosomal pH. Thus, we predict that knock down of CXorf21 expression in primary monocytes may recapitulate what was observed with manipulation of Slc15a4 expression.
	0.51	CXorf21 knockdown, female monocytes treated with a TLR7 agonist had a 7-fold decrease in IFNA1 expression compared to vehicle-treated cells transfected with control gRNA and knockdown of CXorf21 diminished this effect (Figure 5A).
31092820	0.98	CXORF21 protein colocalises with TLR7, a pathway implicated in SLE pathogenesis.
	0.98	CXorf21 is one of eighteen X chromosome genes (including TLR7, IL13RA1 and ELF4) which were up-regulated in response to IFN-alpha stimulation (fold-change: 2.41; P = 6.0 x 10-9; ANOVA; Fig. 5a).
	0.98	CXorf21 correlated with the Toll-like receptor (TLR) signalling pathway including TLR7, TLR6, PIK3CG and PIK3CD (Supplementary Table 5), of which TLR7 was highest ranked.
	0.98	CXorf21 and TLR7, was replicated in TwinsUK RNA-Seq data from LCLs from non-skewed females (n = 271; rho = 0.38; P = 6 x 10-11).
	0.98	CXORF21 and TLR7.
	0.98	TLR7 and CXORF21 in ex vivo B cells.
	0.98	TLR7 staining in the first column, CXORF21 in the second column, DAPI nuclear staining in column three, and in the fourth column all three stains are merged: TLR7 (magenta), CXORF21 (green) and DAPI (blue).
	0.98	CXorf21 with components of the Toll-like receptor signalling pathway (Supplementary Table 6), we utilised the increased resolution of structured illumination microscopy (SIM) to determine whether there was any evidence for colocalisation of CXORF21 with TLR7.
	0.98	CXORF21 and TLR7 were observed after IFN-alpha treatment of resting or IgM/CD40 stimulated B cells.
	0.98	CXORF21) are shown for Ig/CD40 stimulated B cells (Fig. 7a) with exposure to the inhibitor of autophagic flux, bafilomycin (Fig. 7b) and Ig/TLR7/8 stimulated B cells (Fig. 7c) with bafilomycin (Fig. 7d).
	0.98	CXORF21 with TLR7 in B cells.
	0.98	TLR7 and CXorf21 at the RNA level.
	0.98	CXORF21 and TLR7 may interact within these compartments is not clear on the basis of our data, but further exploration of this question should reveal more insights into the function of CXORF21 and how it promotes systemic autoimmunity.
	0.97	TLR7 and CXORF21 are shown from Z-stack images from single B cells (represented as open circles).
	0.97	TLR7, TMEM187, IRAK1, and CXorf21).
	0.94	CXORF21 co-localisation with TLR7; a gene causatively linked to SLE and which also evades XCI.
31001245	0.98	CXorf21 with CRISPR-Cas resulted in abrogation of interferon, TNF-alpha and IL6 secretion after TLR7 activation in female cells.
	0.98	TLR7 signaling, our data using CXorf21 CRISPR-Cas knockdown show that there is a loss of TLR7 agonist-induced increased TLR7 expression (both mRNA and protein).
	0.98	CXorf21, Slc15a4, TLR7, and NCF1 (encodes the p47phox NOX2 subunit) all contain SLE risk alleles.
	0.98	CXorf21 also regulates this pH. NOX2 is activated by phosphorylation of its p47phox subunit by TLR7 signaling.
	0.98	TLR7 and NOX2 signaling are both regulated by endolysosomal pH, and activated NOX2 regulates endolysosomal pH. Both CXorf21 and TLR7 escape X inactivation.
	0.97	CXorf21 and TLR7 expression, have a more favorable lysosomal processing environment compared to male cells, and may drive the robust TLRs/lysosomal-dependent immune response observed women compared to men.
	0.97	CXorf21 is critically involved in TLR7 signaling, including a feedforward expression loop for TLR7.
	0.97	CXorf21, which form a complex that regulates lysosomal pH, and in turn regulates TLR7 signaling.
	0.96	CXorf21 knockdown using small guide RNA resulted in an abrogation of interferon production after exposure of female cells to TLR7 agonist.
	0.89	CXorf21, either because of the presence of two X chromosomes and the escape of X inactivation, or because the SLE-risk allele increases expression, leads to increased TLR7 signaling and increased interferon production.
27933432	0.98	CXorf21, MECP2, and IRAK1 as well as TLR7 and TLR8 (Table 1).
29316339	0.98	TLR7 and CXorf21, both of which escape X inactivation in various immune cells.