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The Role of T Follicular Helper Cells and T Follicular Regulatory Cells in the Pathogenesis of Autoimmune Hemolytic Anemia
Autoimmune hemolytic anemia (AIHA) is an acquired autoimmune disease mediated by antibodies against the patient’s red blood cells. However, the underlying mechanisms for antibody production are not fully understood. Previous studies of etiology and pathogenesis of AIHA mainly focus on autoreactive B...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6930209/ https://www.ncbi.nlm.nih.gov/pubmed/31875006 http://dx.doi.org/10.1038/s41598-019-56365-3 |
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author | Gao, Yuhan Jin, Haiqiang Nan, Ding Yu, Weiwei Zhang, Jianhua Yang, Ying Hou, Ruiqin Qin, Ranran Hao, Hongjun Sun, Yongan Tian, Wenqin |
author_facet | Gao, Yuhan Jin, Haiqiang Nan, Ding Yu, Weiwei Zhang, Jianhua Yang, Ying Hou, Ruiqin Qin, Ranran Hao, Hongjun Sun, Yongan Tian, Wenqin |
author_sort | Gao, Yuhan |
collection | PubMed |
description | Autoimmune hemolytic anemia (AIHA) is an acquired autoimmune disease mediated by antibodies against the patient’s red blood cells. However, the underlying mechanisms for antibody production are not fully understood. Previous studies of etiology and pathogenesis of AIHA mainly focus on autoreactive B cells that have escaped tolerance mechanisms. Few studies have reported the function of T(FH) and T(FR) cells in the process of AIHA. The present study aimed to explore the potential mechanism of T(FH) and T(FR) cells in the pathogenesis of AIHA. With the model of murine AIHA, increased ratios of T(FH):T(FR), elevated serum IL-21 and IL-6 levels, and upregulated Bcl-6 and c-Maf expression were reported. Also, adoptive transfer of purified CD4(+)CXCR5(+)CD25(-) T cells from immunized mice promoted the induction of autoantibody in the AIHA mouse model. Altogether, our data demonstrate the important role of T(FH) cells for control and induction of AIHA. In the light of the key contributions of T(FH) cells to the immune response in AIHA, strategies aimed at inhibiting the T(FH) development or function should be emphasized. |
format | Online Article Text |
id | pubmed-6930209 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-69302092019-12-27 The Role of T Follicular Helper Cells and T Follicular Regulatory Cells in the Pathogenesis of Autoimmune Hemolytic Anemia Gao, Yuhan Jin, Haiqiang Nan, Ding Yu, Weiwei Zhang, Jianhua Yang, Ying Hou, Ruiqin Qin, Ranran Hao, Hongjun Sun, Yongan Tian, Wenqin Sci Rep Article Autoimmune hemolytic anemia (AIHA) is an acquired autoimmune disease mediated by antibodies against the patient’s red blood cells. However, the underlying mechanisms for antibody production are not fully understood. Previous studies of etiology and pathogenesis of AIHA mainly focus on autoreactive B cells that have escaped tolerance mechanisms. Few studies have reported the function of T(FH) and T(FR) cells in the process of AIHA. The present study aimed to explore the potential mechanism of T(FH) and T(FR) cells in the pathogenesis of AIHA. With the model of murine AIHA, increased ratios of T(FH):T(FR), elevated serum IL-21 and IL-6 levels, and upregulated Bcl-6 and c-Maf expression were reported. Also, adoptive transfer of purified CD4(+)CXCR5(+)CD25(-) T cells from immunized mice promoted the induction of autoantibody in the AIHA mouse model. Altogether, our data demonstrate the important role of T(FH) cells for control and induction of AIHA. In the light of the key contributions of T(FH) cells to the immune response in AIHA, strategies aimed at inhibiting the T(FH) development or function should be emphasized. Nature Publishing Group UK 2019-12-24 /pmc/articles/PMC6930209/ /pubmed/31875006 http://dx.doi.org/10.1038/s41598-019-56365-3 Text en © The Author(s) 2019 Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Gao, Yuhan Jin, Haiqiang Nan, Ding Yu, Weiwei Zhang, Jianhua Yang, Ying Hou, Ruiqin Qin, Ranran Hao, Hongjun Sun, Yongan Tian, Wenqin The Role of T Follicular Helper Cells and T Follicular Regulatory Cells in the Pathogenesis of Autoimmune Hemolytic Anemia |
title | The Role of T Follicular Helper Cells and T Follicular Regulatory Cells in the Pathogenesis of Autoimmune Hemolytic Anemia |
title_full | The Role of T Follicular Helper Cells and T Follicular Regulatory Cells in the Pathogenesis of Autoimmune Hemolytic Anemia |
title_fullStr | The Role of T Follicular Helper Cells and T Follicular Regulatory Cells in the Pathogenesis of Autoimmune Hemolytic Anemia |
title_full_unstemmed | The Role of T Follicular Helper Cells and T Follicular Regulatory Cells in the Pathogenesis of Autoimmune Hemolytic Anemia |
title_short | The Role of T Follicular Helper Cells and T Follicular Regulatory Cells in the Pathogenesis of Autoimmune Hemolytic Anemia |
title_sort | role of t follicular helper cells and t follicular regulatory cells in the pathogenesis of autoimmune hemolytic anemia |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6930209/ https://www.ncbi.nlm.nih.gov/pubmed/31875006 http://dx.doi.org/10.1038/s41598-019-56365-3 |
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