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Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus
Systemic lupus erythematosus (SLE) is an autoimmune illness marked by the loss of immune tolerance and the production of autoantibodies against nucleic acids and other nuclear antigens (Ags). B lymphocytes are important in the immunopathogenesis of SLE. Multiple receptors control abnormal B-cell act...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975558/ https://www.ncbi.nlm.nih.gov/pubmed/36875095 http://dx.doi.org/10.3389/fimmu.2023.1093208 |
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author | Wen, Luyao Zhang, Bei Wu, Xinfeng Liu, Rongzeng Fan, Hua Han, Lei Zhang, Zhibo Ma, Xin Chu, Cong-Qiu Shi, Xiaofei |
author_facet | Wen, Luyao Zhang, Bei Wu, Xinfeng Liu, Rongzeng Fan, Hua Han, Lei Zhang, Zhibo Ma, Xin Chu, Cong-Qiu Shi, Xiaofei |
author_sort | Wen, Luyao |
collection | PubMed |
description | Systemic lupus erythematosus (SLE) is an autoimmune illness marked by the loss of immune tolerance and the production of autoantibodies against nucleic acids and other nuclear antigens (Ags). B lymphocytes are important in the immunopathogenesis of SLE. Multiple receptors control abnormal B-cell activation in SLE patients, including intrinsic Toll-like receptors (TLRs), B-cell receptors (BCRs), and cytokine receptors. The role of TLRs, notably TLR7 and TLR9, in the pathophysiology of SLE has been extensively explored in recent years. When endogenous or exogenous nucleic acid ligands are recognized by BCRs and internalized into B cells, they bind TLR7 or TLR9 to activate related signalling pathways and thus govern the proliferation and differentiation of B cells. Surprisingly, TLR7 and TLR9 appear to play opposing roles in SLE B cells, and the interaction between them is still poorly understood. In addition, other cells can enhance TLR signalling in B cells of SLE patients by releasing cytokines that accelerate the differentiation of B cells into plasma cells. Therefore, the delineation of how TLR7 and TLR9 regulate the abnormal activation of B cells in SLE may aid the understanding of the mechanisms of SLE and provide directions for TLR-targeted therapies for SLE. |
format | Online Article Text |
id | pubmed-9975558 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-99755582023-03-02 Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus Wen, Luyao Zhang, Bei Wu, Xinfeng Liu, Rongzeng Fan, Hua Han, Lei Zhang, Zhibo Ma, Xin Chu, Cong-Qiu Shi, Xiaofei Front Immunol Immunology Systemic lupus erythematosus (SLE) is an autoimmune illness marked by the loss of immune tolerance and the production of autoantibodies against nucleic acids and other nuclear antigens (Ags). B lymphocytes are important in the immunopathogenesis of SLE. Multiple receptors control abnormal B-cell activation in SLE patients, including intrinsic Toll-like receptors (TLRs), B-cell receptors (BCRs), and cytokine receptors. The role of TLRs, notably TLR7 and TLR9, in the pathophysiology of SLE has been extensively explored in recent years. When endogenous or exogenous nucleic acid ligands are recognized by BCRs and internalized into B cells, they bind TLR7 or TLR9 to activate related signalling pathways and thus govern the proliferation and differentiation of B cells. Surprisingly, TLR7 and TLR9 appear to play opposing roles in SLE B cells, and the interaction between them is still poorly understood. In addition, other cells can enhance TLR signalling in B cells of SLE patients by releasing cytokines that accelerate the differentiation of B cells into plasma cells. Therefore, the delineation of how TLR7 and TLR9 regulate the abnormal activation of B cells in SLE may aid the understanding of the mechanisms of SLE and provide directions for TLR-targeted therapies for SLE. Frontiers Media S.A. 2023-02-15 /pmc/articles/PMC9975558/ /pubmed/36875095 http://dx.doi.org/10.3389/fimmu.2023.1093208 Text en Copyright © 2023 Wen, Zhang, Wu, Liu, Fan, Han, Zhang, Ma, Chu and Shi https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Wen, Luyao Zhang, Bei Wu, Xinfeng Liu, Rongzeng Fan, Hua Han, Lei Zhang, Zhibo Ma, Xin Chu, Cong-Qiu Shi, Xiaofei Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus |
title | Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus |
title_full | Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus |
title_fullStr | Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus |
title_full_unstemmed | Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus |
title_short | Toll-like receptors 7 and 9 regulate the proliferation and differentiation of B cells in systemic lupus erythematosus |
title_sort | toll-like receptors 7 and 9 regulate the proliferation and differentiation of b cells in systemic lupus erythematosus |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9975558/ https://www.ncbi.nlm.nih.gov/pubmed/36875095 http://dx.doi.org/10.3389/fimmu.2023.1093208 |
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