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Gene Information
Gene symbol: ICOSLG
Gene name: inducible T-cell co-stimulator ligand
HGNC ID: 17087
Synonyms: KIAA0653, GL50, B7-H2, B7RP-1, B7H2, B7RP1, ICOS-L, CD275
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | CCNY | 1 hits |
| 2 | HERC2 | 1 hits |
| 3 | ICOS | 1 hits |
| 4 | IL10 | 1 hits |
| 5 | IL12B | 1 hits |
| 6 | IL1R2 | 1 hits |
| 7 | IL23A | 1 hits |
| 8 | IL23R | 1 hits |
| 9 | IL26 | 1 hits |
| 10 | JAK2 | 1 hits |
| 11 | NKX2-3 | 1 hits |
| 12 | ORMDL3 | 1 hits |
| 13 | REL | 1 hits |
| 14 | SMAD3 | 1 hits |
| 15 | STAT3 | 1 hits |
| 16 | TNFAIP3 | 1 hits |
| 17 | TNFSF15 | 1 hits |
| 18 | TYK2 | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 20176734 | We identified multiple previously unreported or unconfirmed disease associations, including known CD loci (ICOSLG and TNFSF15) and T1D loci (TNFAIP3) that confer UC risk, known UC loci (HERC2 and IL26) that confer T1D risk and known UC loci (IL10 and CCNY) that confer CD risk. |
| 2 | 20176734 | Additionally, we show that T1D risk alleles residing at the PTPN22, IL27, IL18RAP and IL10 loci protect against CD. |
| 3 | 20544729 | In this study, we provide evidence that the Icos and Icosl genes contribute to the diabetes process. |
| 4 | 20544729 | Protection from diabetes in ICOS(-/-) and ICOSL(-/-) NOD mice was unexpectedly associated with the development of an autoimmune disorder of the neuro-muscular system, characterized by myositis, sensory ganglionitis and, to a reduced extent, inflammatory infiltrates in the CNS. |
| 5 | 20544729 | This syndrome was reproduced upon adoptive transfer of CD4(+) and CD8(+) T cells from diseased donors to naïve NOD.scid recipients. |
| 6 | 20544729 | Taken together, our findings indicate that costimulation signals play a key role in regulating immune tolerance in peripheral tissues and that the ICOS/ICOSL costimulatory pathway influences the balance between Treg and diabetogenic effector T cells. |
| 7 | 20544729 | In this study, we provide evidence that the Icos and Icosl genes contribute to the diabetes process. |
| 8 | 20544729 | Protection from diabetes in ICOS(-/-) and ICOSL(-/-) NOD mice was unexpectedly associated with the development of an autoimmune disorder of the neuro-muscular system, characterized by myositis, sensory ganglionitis and, to a reduced extent, inflammatory infiltrates in the CNS. |
| 9 | 20544729 | This syndrome was reproduced upon adoptive transfer of CD4(+) and CD8(+) T cells from diseased donors to naïve NOD.scid recipients. |
| 10 | 20544729 | Taken together, our findings indicate that costimulation signals play a key role in regulating immune tolerance in peripheral tissues and that the ICOS/ICOSL costimulatory pathway influences the balance between Treg and diabetogenic effector T cells. |
| 11 | 20544729 | In this study, we provide evidence that the Icos and Icosl genes contribute to the diabetes process. |
| 12 | 20544729 | Protection from diabetes in ICOS(-/-) and ICOSL(-/-) NOD mice was unexpectedly associated with the development of an autoimmune disorder of the neuro-muscular system, characterized by myositis, sensory ganglionitis and, to a reduced extent, inflammatory infiltrates in the CNS. |
| 13 | 20544729 | This syndrome was reproduced upon adoptive transfer of CD4(+) and CD8(+) T cells from diseased donors to naïve NOD.scid recipients. |
| 14 | 20544729 | Taken together, our findings indicate that costimulation signals play a key role in regulating immune tolerance in peripheral tissues and that the ICOS/ICOSL costimulatory pathway influences the balance between Treg and diabetogenic effector T cells. |
| 15 | 21300624 | Amongst these are multiple genes involved in IL23/Th17 signalling (IL23R, IL12B, JAK2, TYK2 and STAT3), IL10, IL1R2, REL, CARD9, NKX2.3, ICOSLG, PRDM1, SMAD3 and ORMDL3. |
| 16 | 21300624 | For Crohn's disease, defective processing of intracellular bacteria has become a central theme, following gene discoveries in autophagy and innate immunity (associations with NOD2, IRGM, ATG16L1 are specific to Crohn's disease). |
| 17 | 21300624 | Genetic evidence has also demonstrated the importance of barrier function to the development of ulcerative colitis (HNF4A, LAMB1, CDH1 and GNA12). |