Ignet

Gene Information

Gene symbol: IL23R

Gene name: interleukin 23 receptor

HGNC ID: 19100

Synonyms: IL-23R

Related Genes

#	Gene Symbol	Number of hits
1	CXCR3	1 hits
2	ICOS	1 hits
3	IFNG	1 hits
4	IL12A	1 hits
5	IL17D	1 hits
6	IL22	1 hits
7	IL23A	1 hits
8	IL9	1 hits

Related Sentences

#	PMID	Sentence
1	20171917	Bacille Calmette-Guérin infection and disease with fatal outcome associated with a point mutation in the interleukin-12/interleukin-23 receptor beta-1 chain in two Mexican families.
2	20171917	The β1 subunit of the IL-12 receptor (encoded by the IL12RB1 gene) was not expressed in cells from P1 or P2, or in two siblings of P1.
3	20171917	Doctors must be alert to the adverse reactions to BCG vaccination and to persistent Mycobacterium infections, and in such cases should investigate possible mutations in the genes of the IL-12/IL-23-IFN-γ axis.
4	20504940	Interleukin-22 (IL-22) production by pulmonary Natural Killer cells and the potential role of IL-22 during primary influenza virus infection.
5	20504940	We set out to test the hypothesis that interleukin-22 (IL-22), a cytokine crucial for epithelial cell homeostasis and recovery from tissue injury, would be protective during influenza virus infection.
6	20504940	Recent studies have identified phenotypically and functionally unique intestinal NK cells capable of producing the cytokine IL-22.
7	20504940	Unlike gut NK cells that produce IL-22, the surface phenotypes of lung NK cells were similar to those of spleen NK cells and were characteristically mature.
8	20504940	With mitogen stimulation, both single and double IL-22- and gamma interferon (IFN-gamma)-producing lung NK cells were detected.
9	20504940	However, only the IL-22(+) IFN-gamma(-) lung NK subset was observed after stimulation with IL-23.
10	20504940	IL-23 receptor (IL-23R) blocking dramatically inhibited IL-22 production, but not IFN-gamma production.
11	20504940	Furthermore, we found that NK1.1(+) or CD27(-) lung NK cells were the primary sources of IL-22.
12	20504940	After influenza virus infection, lung NK cells were quickly activated to produce both IFN-gamma and IL-22 and had increased cytotoxic potential.
13	20504940	The level of IL-22 in the lung tissue declined shortly after infection, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was maintained.
14	20504940	Furthermore, depletion of NK cells with or without influenza virus infection reduced the protein level of IL-22 in the lung.
15	20504940	Our data suggest that during primary respiratory viral infection, IL-22 seems to a play a marginal role for protection, indicating a differential requirement of this cytokine for bacterial and viral infections.
16	22772464	We determined that T cells from mice deficient in the T helper type 17 (T(H)17) pathway genes encoding retinoid-related orphan receptor γ (ROR-γ) and IL-23 receptor (IL-23R) produced abundant IL-9, and we found substantial growth inhibition of B16F10 melanoma in these mice.
17	22772464	Il9r(-/-) mice showed accelerated tumor growth, and administration of recombinant IL-9 (rIL-9) to tumor-bearing WT and Rag1(-/-) mice inhibited melanoma as well as lung carcinoma growth.
18	25576595	The inducible costimulator (ICOS) plays a key role in the development of Th17 cells, but its role in the development and antitumor activity of IL-17-producing CD8(+) T cells (Tc17) remains unknown.
19	25576595	However, ICOS stimulation did not augment the antitumor activity of IL-2 expanded T cells.
20	25576595	Additional investigation revealed that ICOS stimulation not only increased IL-2Rα, CXCR3, and IL-23R expression on Tc17 cells, but also dampened their expression of suppressive molecule CD39.
21	25576595	Although Tc17 cells activated with an ICOS agonist cosecreted heightened IL-17A, IL-9, and IFN-γ, their therapeutic effectiveness was critically dependent on IFN-γ production.
22	25576595	Depletion of IL-17A and IL-9 had little impact on antitumor Tc17 cells activated with an ICOS agonist.