Antigen-Specific CD25 − Foxp3 − IFN-γ high CD4 + T Cells Restrain the Development of Experimental Allergic Encephalomyelitis by Suppressing Th17
The American Journal of Pathology, ISSN: 0002-9440, Vol: 176, Issue: 6, Page: 2764-2775
2010
- 14Citations
- 25Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations14
- Citation Indexes14
- 14
- CrossRef13
- Captures25
- Readers25
- 25
Article Description
The current study identifies within the Th1 subtype two distinct CD4 + populations: those capable of transferring inflammatory autoimmunity and others that regulate its development by suppressing Th17 in an interferon (IFN)-γ-dependent manner. These CD4 + IFN-γ high IL-4 low IL-10 low TGF-β low FOXp3 − cells in fact function as antigen-specific regulatory cells that restrain the development of autoimmunity by increasing the threshold of Th17 activation. We show that development of autoimmune conditions within the central nervous system is dependent on the Fas ligand-mediated apoptosis of these regulatory cells at early stages of disease. We also show that not only is the function of these cells IFN-γ dependent but also that stable over expression of IFN-γ in encephalitogenic CD4 + T cells redirects their biological function to become antigen-specific regulatory cells. This may also explain, in part, the pleiotropic role of IFN-γ in the regulation of autoimmunity, as previously observed by others.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0002944010607985; http://dx.doi.org/10.2353/ajpath.2010.090855; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77953210389&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/20382706; https://linkinghub.elsevier.com/retrieve/pii/S0002944010607985; http://ajp.amjpathol.org/article/S0002-9440(10)60798-5/abstract
Elsevier BV
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