ArticleThe American journal of pathology2010
Antigen-specific CD25- Foxp3- IFN-gamma(high) CD4+ T cells restrain the development of experimental allergic encephalomyelitis by suppressing Th17.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Bidirectional Effect of IFN-γ on Th17 Responses in Experimental Autoimmune Uveitis.Frontiers in ophthalmology · 2022Article
- Current prospects of type II interferon γ signaling and autoimmunity.The Journal of biological chemistry · 2017Review
- CCR8Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Chronic exposure to trichloroethylene increases DNA methylation of the Ifng promoter in CD4Toxicology letters · 2016Article
- T cell subsets and their signature cytokines in autoimmune and inflammatory diseases.Cytokine · 2015Review
- Stage-Specific Role of Interferon-Gamma in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis.Frontiers in immunology · 2015Review
- CXCL11-dependent induction of FOXP3-negative regulatory T cells suppresses autoimmune encephalomyelitis.The Journal of clinical investigation · 2014Article
- Interferon-gamma negatively regulates Th17-mediated immunopathology during mouse hepatitis virus infection.Journal of molecular medicine (Berlin, Germany) · 2011Article
- Interleukin-27 and interferon-gamma are involved in regulation of autoimmune arthritis.The Journal of biological chemistry · 2011Article
Corrections and comments
- Commented on byCorrection.2017
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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)-gamma-dependent manner. These CD4(+)IFN-gamma(high)IL-4(low)IL-10(low)TGF-beta(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-gamma dependent but also that stable over expression of IFN-gamma 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-gamma in the regulation of autoimmunity, as previously observed by others.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.