 | Draft article not currently submitted for review.
This is a draft Articles for creation (AfC) submission. It is not currently pending review. While there are no deadlines, abandoned drafts may be deleted after six months. To edit the draft click on the "Edit" tab at the top of the window. To be accepted, a draft should:
It is strongly discouraged to write about yourself, your business or employer. If you do so, you must declare it. Where to get help
How to improve a draft
You can also browse Wikipedia:Featured articles and Wikipedia:Good articles to find examples of Wikipedia's best writing on topics similar to your proposed article. Improving your odds of a speedy review To improve your odds of a faster review, tag your draft with relevant WikiProject tags using the button below. This will let reviewers know a new draft has been submitted in their area of interest. For instance, if you wrote about a female astronomer, you would want to add the Biography, Astronomy, and Women scientists tags. Editor resources
Last edited by Citation bot (talk | contribs) 3 seconds ago. (Update) |
| Inducible T-cell CO-Stimulator Ligand (ICOS-L) | |||||||||
|---|---|---|---|---|---|---|---|---|---|
| Identifiers | |||||||||
| Symbol | ICOSLG | ||||||||
| Pfam | PF07686 | ||||||||
| Pfam clan | CL0159 | ||||||||
| InterPro | IPR013162 | ||||||||
| SMART | SM00262 | ||||||||
| PROSITE | PS01216 | ||||||||
| SCOP2 | 1cdp / SCOPe / SUPFAM | ||||||||
| OPM superfamily | 190 | ||||||||
| CDD | cd16052 | ||||||||
| |||||||||
The Inducible T-cell CO-Stimulator Ligand (ICOS-L), also known as B7-H2 or CD275, is a protein that in humans is encoded by the ICOSLG gene. It plays a crucial role in the regulation of immune responses, particularly in the activation and differentiation of T cells.[1]
Function
editICOS-L is a member of the B7 family of co-stimulatory molecules, expressed on antigen-presenting cells (APCs) such as B cells, macrophages, and dendritic cells. It binds to the ICOS receptor on T cells, playing a critical role in their activation, survival, and function. This interaction is essential for the formation of germinal centers, which are crucial for the production of high-affinity antibodies.[2]
Expression
editICOS-L is widely expressed not only on APCs but also on non-immune cells such as epithelial cells, fibroblasts, and keratinocytes. The expression of ICOS-L can be upregulated in response to inflammatory stimuli, making it a key player in chronic inflammatory conditions and autoimmune diseases.[3]
Clinical Significance
editDysregulation of the ICOS-ICOS-L pathway is associated with various autoimmune diseases, including rheumatoid arthritis (RA). In RA, the ICOS/ICOS-L interaction contributes to the activation of autoreactive T cells and the production of inflammatory cytokines, exacerbating the disease. Therapeutic targeting of this pathway, such as with ICOS-L blocking antibodies, has shown potential in reducing disease severity by modulating immune responses.[4][5]
References
edit- ^ Smith KM (2006). "ICOS Ligand (B7-H2) as a potential therapeutic target for immune disorders". Journal of Immunology. 176 (1): 18–26. doi:10.4049/jimmunol.176.1.18 (inactive 1 November 2024).
{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link) - ^ Greenwald RJ (2005). "The B7 family revisited". Annual Review of Immunology. 23: 515–548. doi:10.1146/annurev.immunol.23.021704.115611. PMID 15771580.
- ^ Iwai Y (2020). "Involvement of the ICOS pathway in the pathogenesis of autoimmune diseases". Frontiers in Immunology. 10: 456. doi:10.3389/fimmu.2020.00456. PMC 7137904. PMID 32296418.
- ^ Qi H (2019). "T-cell help in germinal centers controlled by ICOSL-ICOS co-stimulation". Nature Reviews Drug Discovery. 18: 801–816. doi:10.1038/s41573-019-0032-6 (inactive 1 November 2024).
{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link) - ^ Hansson GK (2020). "ICOSL blockade as a therapeutic strategy in autoimmunity". Nature Reviews Drug Discovery. 19 (3): 112–123. doi:10.1038/s41573-020-00030-5 (inactive 1 November 2024).
{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)