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Immune regulation in renal inflammation
Renal inflammation, induced by autoantigen recognition or toxic drugs, leads to renal tissue injury and decline in kidney function. Recent studies have demonstrated the crucial role for regulatory T cells in suppressing pathogenic adaptive but also innate immune responses in the inflamed kidney. How...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8523435/ https://www.ncbi.nlm.nih.gov/pubmed/33496881 http://dx.doi.org/10.1007/s00441-020-03351-1 |
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author | Neumann, Katrin Tiegs, Gisa |
author_facet | Neumann, Katrin Tiegs, Gisa |
author_sort | Neumann, Katrin |
collection | PubMed |
description | Renal inflammation, induced by autoantigen recognition or toxic drugs, leads to renal tissue injury and decline in kidney function. Recent studies have demonstrated the crucial role for regulatory T cells in suppressing pathogenic adaptive but also innate immune responses in the inflamed kidney. However, there is also evidence for other immune cell populations with immunosuppressive function in renal inflammation. This review summarizes mechanisms of immune cell regulation in immune-mediated glomerulonephritis and acute and chronic nephrotoxicity. |
format | Online Article Text |
id | pubmed-8523435 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-85234352021-11-04 Immune regulation in renal inflammation Neumann, Katrin Tiegs, Gisa Cell Tissue Res Review Renal inflammation, induced by autoantigen recognition or toxic drugs, leads to renal tissue injury and decline in kidney function. Recent studies have demonstrated the crucial role for regulatory T cells in suppressing pathogenic adaptive but also innate immune responses in the inflamed kidney. However, there is also evidence for other immune cell populations with immunosuppressive function in renal inflammation. This review summarizes mechanisms of immune cell regulation in immune-mediated glomerulonephritis and acute and chronic nephrotoxicity. Springer Berlin Heidelberg 2021-01-26 2021 /pmc/articles/PMC8523435/ /pubmed/33496881 http://dx.doi.org/10.1007/s00441-020-03351-1 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Review Neumann, Katrin Tiegs, Gisa Immune regulation in renal inflammation |
title | Immune regulation in renal inflammation |
title_full | Immune regulation in renal inflammation |
title_fullStr | Immune regulation in renal inflammation |
title_full_unstemmed | Immune regulation in renal inflammation |
title_short | Immune regulation in renal inflammation |
title_sort | immune regulation in renal inflammation |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8523435/ https://www.ncbi.nlm.nih.gov/pubmed/33496881 http://dx.doi.org/10.1007/s00441-020-03351-1 |
work_keys_str_mv | AT neumannkatrin immuneregulationinrenalinflammation AT tiegsgisa immuneregulationinrenalinflammation |