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Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases
Toll-like receptors (TLRs) comprise a class of highly conserved molecules that recognize pathogen-associated molecular patterns and play a vital role in host defense against multiple viral infectious diseases. Although TLRs are highly expressed on innate immune cells and play indirect roles in regul...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9555683/ https://www.ncbi.nlm.nih.gov/pubmed/36224474 http://dx.doi.org/10.1007/s00018-022-04582-x |
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author | Zhang, Ejuan Ma, Zhiyong Lu, Mengji |
author_facet | Zhang, Ejuan Ma, Zhiyong Lu, Mengji |
author_sort | Zhang, Ejuan |
collection | PubMed |
description | Toll-like receptors (TLRs) comprise a class of highly conserved molecules that recognize pathogen-associated molecular patterns and play a vital role in host defense against multiple viral infectious diseases. Although TLRs are highly expressed on innate immune cells and play indirect roles in regulating antiviral adaptive immune responses, intrinsic expression of TLRs in adaptive immune cells, including T cells and B cells, cannot be ignored. TLRs expressed in CD4 + and CD8 + T cells play roles in enhancing TCR signal-induced T-cell activation, proliferation, function, and survival, serving as costimulatory molecules. Gene knockout of TLR signaling molecules has been shown to diminish antiviral adaptive immune responses and affect viral clearance in multiple viral infectious animal models. These results have highlighted the critical role of TLRs in the long-term immunological control of viral infection. This review summarizes the expression and function of TLR signaling pathways in T and B cells, focusing on the in vitro and vivo mechanisms and effects of intrinsic TLR signaling in regulating T- and B-cell responses during viral infection. The potential clinical use of TLR-based immune regulatory drugs for viral infectious diseases is also explored. |
format | Online Article Text |
id | pubmed-9555683 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-95556832022-10-13 Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases Zhang, Ejuan Ma, Zhiyong Lu, Mengji Cell Mol Life Sci Review Toll-like receptors (TLRs) comprise a class of highly conserved molecules that recognize pathogen-associated molecular patterns and play a vital role in host defense against multiple viral infectious diseases. Although TLRs are highly expressed on innate immune cells and play indirect roles in regulating antiviral adaptive immune responses, intrinsic expression of TLRs in adaptive immune cells, including T cells and B cells, cannot be ignored. TLRs expressed in CD4 + and CD8 + T cells play roles in enhancing TCR signal-induced T-cell activation, proliferation, function, and survival, serving as costimulatory molecules. Gene knockout of TLR signaling molecules has been shown to diminish antiviral adaptive immune responses and affect viral clearance in multiple viral infectious animal models. These results have highlighted the critical role of TLRs in the long-term immunological control of viral infection. This review summarizes the expression and function of TLR signaling pathways in T and B cells, focusing on the in vitro and vivo mechanisms and effects of intrinsic TLR signaling in regulating T- and B-cell responses during viral infection. The potential clinical use of TLR-based immune regulatory drugs for viral infectious diseases is also explored. Springer International Publishing 2022-10-12 2022 /pmc/articles/PMC9555683/ /pubmed/36224474 http://dx.doi.org/10.1007/s00018-022-04582-x Text en © The Author(s) 2022 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 Zhang, Ejuan Ma, Zhiyong Lu, Mengji Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases |
title | Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases |
title_full | Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases |
title_fullStr | Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases |
title_full_unstemmed | Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases |
title_short | Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases |
title_sort | contribution of t- and b-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9555683/ https://www.ncbi.nlm.nih.gov/pubmed/36224474 http://dx.doi.org/10.1007/s00018-022-04582-x |
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