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CD4(+) T-Cell Plasticity in Non-Infectious Retinal Inflammatory Disease
Non-infectious uveitis (NIU) is a potentially sight-threatening disease. Effector CD4(+) T cells, especially interferon-γ-(IFNγ) producing Th1 cells and interleukin-17-(IL-17) producing Th17 cells, are the major immunopathogenic cells, as demonstrated by adoptive transfer of disease in a model of ex...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8431487/ https://www.ncbi.nlm.nih.gov/pubmed/34502490 http://dx.doi.org/10.3390/ijms22179584 |
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author | Chen, Yi-Hsing Lightman, Sue Calder, Virginia L. |
author_facet | Chen, Yi-Hsing Lightman, Sue Calder, Virginia L. |
author_sort | Chen, Yi-Hsing |
collection | PubMed |
description | Non-infectious uveitis (NIU) is a potentially sight-threatening disease. Effector CD4(+) T cells, especially interferon-γ-(IFNγ) producing Th1 cells and interleukin-17-(IL-17) producing Th17 cells, are the major immunopathogenic cells, as demonstrated by adoptive transfer of disease in a model of experimental autoimmune uveitis (EAU). CD4(+)FoxP3(+)CD25(+) regulatory T cells (Tregs) were known to suppress function of effector CD4(+) T cells and contribute to resolution of disease. It has been recently reported that some CD4(+) T-cell subsets demonstrate shared phenotypes with another CD4(+) T-cell subset, offering the potential for dual function. For example, Th17/Th1 (co-expressing IFNγ and IL-17) cells and Th17/Treg (co-expressing IL-17 and FoxP3) cells have been identified in NIU and EAU. In this review, we have investigated the evidence as to whether these ‘plastic CD4(+) T cells’ are functionally active in uveitis. We conclude that Th17/Th1 cells are generated locally, are resistant to the immunosuppressive effects of steroids, and contribute to early development of EAU. Th17/Treg cells produce IL-17, not IL-10, and act similar to Th17 cells. These cells were considered pathogenic in uveitis. Future studies are needed to better clarify their function, and in the future, these cell subsets may in need to be taken into consideration for designing treatment strategies for disease. |
format | Online Article Text |
id | pubmed-8431487 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-84314872021-09-11 CD4(+) T-Cell Plasticity in Non-Infectious Retinal Inflammatory Disease Chen, Yi-Hsing Lightman, Sue Calder, Virginia L. Int J Mol Sci Review Non-infectious uveitis (NIU) is a potentially sight-threatening disease. Effector CD4(+) T cells, especially interferon-γ-(IFNγ) producing Th1 cells and interleukin-17-(IL-17) producing Th17 cells, are the major immunopathogenic cells, as demonstrated by adoptive transfer of disease in a model of experimental autoimmune uveitis (EAU). CD4(+)FoxP3(+)CD25(+) regulatory T cells (Tregs) were known to suppress function of effector CD4(+) T cells and contribute to resolution of disease. It has been recently reported that some CD4(+) T-cell subsets demonstrate shared phenotypes with another CD4(+) T-cell subset, offering the potential for dual function. For example, Th17/Th1 (co-expressing IFNγ and IL-17) cells and Th17/Treg (co-expressing IL-17 and FoxP3) cells have been identified in NIU and EAU. In this review, we have investigated the evidence as to whether these ‘plastic CD4(+) T cells’ are functionally active in uveitis. We conclude that Th17/Th1 cells are generated locally, are resistant to the immunosuppressive effects of steroids, and contribute to early development of EAU. Th17/Treg cells produce IL-17, not IL-10, and act similar to Th17 cells. These cells were considered pathogenic in uveitis. Future studies are needed to better clarify their function, and in the future, these cell subsets may in need to be taken into consideration for designing treatment strategies for disease. MDPI 2021-09-03 /pmc/articles/PMC8431487/ /pubmed/34502490 http://dx.doi.org/10.3390/ijms22179584 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Chen, Yi-Hsing Lightman, Sue Calder, Virginia L. CD4(+) T-Cell Plasticity in Non-Infectious Retinal Inflammatory Disease |
title | CD4(+) T-Cell Plasticity in Non-Infectious Retinal Inflammatory Disease |
title_full | CD4(+) T-Cell Plasticity in Non-Infectious Retinal Inflammatory Disease |
title_fullStr | CD4(+) T-Cell Plasticity in Non-Infectious Retinal Inflammatory Disease |
title_full_unstemmed | CD4(+) T-Cell Plasticity in Non-Infectious Retinal Inflammatory Disease |
title_short | CD4(+) T-Cell Plasticity in Non-Infectious Retinal Inflammatory Disease |
title_sort | cd4(+) t-cell plasticity in non-infectious retinal inflammatory disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8431487/ https://www.ncbi.nlm.nih.gov/pubmed/34502490 http://dx.doi.org/10.3390/ijms22179584 |
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