Induced Overexpression of B Cell-Activating Factor by Triiodothyronine Results in Abnormal B Cell Differentiation in Mice

Breakdown of tolerance and abnormal activation in B cells is an important mechanism in the pathogenesis of Graves’ disease (GD) and high levels of thyroid hormones (THs) can drive the progression of GD. However, the interactions between THs and abnormal activation of B cells in the context of GD are...

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Main Authors: Shu Liu, Guo-Qing Li, Qing-Wei Gu, Jie Wang, Qi Sun, Wen-Sha Gu, Xiao-Ming Mao
Format: Article
Language:English
Published: SAGE Publishing 2023-10-01
Series:Cell Transplantation
Online Access:https://doi.org/10.1177/09636897231204075
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author Shu Liu
Guo-Qing Li
Qing-Wei Gu
Jie Wang
Qi Sun
Wen-Sha Gu
Xiao-Ming Mao
author_facet Shu Liu
Guo-Qing Li
Qing-Wei Gu
Jie Wang
Qi Sun
Wen-Sha Gu
Xiao-Ming Mao
author_sort Shu Liu
collection DOAJ
description Breakdown of tolerance and abnormal activation in B cells is an important mechanism in the pathogenesis of Graves’ disease (GD) and high levels of thyroid hormones (THs) can drive the progression of GD. However, the interactions between THs and abnormal activation of B cells in the context of GD are not well understood. The aim of this study was to investigate B cell-activating factor (BAFF) mediating the cross talk between THs and B cells and the possible underlying mechanisms. A high-level triiodothyronine (T3) mouse model was used to verify T3-mediated induction of overexpression of BAFF and B cell abnormal differentiation. The possible promotion of BAFF overexpression in the mice spleen macrophages during polarization to M1 by T3 was also studied. We showed that high levels of T3 can induce BAFF overexpression and lead to abnormal differentiation of B cells in the mice. While the overexpression of BAFF was observed across many tissue types in the mice, high levels of T3 could induce M1 macrophages polarization by IFN (interferon-gamma)-γ in the spleen of the mice, which in turn generated BAFF overexpression. Our findings provide a novel insight into the interactions between the endocrine and immune systems, as well as provide insight into the role of TH in the pathogenesis of GD.
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spelling doaj.art-07d160a6d51d471bbfd566954c57fc3e2023-10-06T09:03:27ZengSAGE PublishingCell Transplantation1555-38922023-10-013210.1177/09636897231204075Induced Overexpression of B Cell-Activating Factor by Triiodothyronine Results in Abnormal B Cell Differentiation in MiceShu Liu0Guo-Qing Li1Qing-Wei Gu2Jie Wang3Qi Sun4Wen-Sha Gu5Xiao-Ming Mao6Department of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaDepartment of Endocrinology, Nanjing First Hospital, Nanjing Medical University, Nanjing, ChinaBreakdown of tolerance and abnormal activation in B cells is an important mechanism in the pathogenesis of Graves’ disease (GD) and high levels of thyroid hormones (THs) can drive the progression of GD. However, the interactions between THs and abnormal activation of B cells in the context of GD are not well understood. The aim of this study was to investigate B cell-activating factor (BAFF) mediating the cross talk between THs and B cells and the possible underlying mechanisms. A high-level triiodothyronine (T3) mouse model was used to verify T3-mediated induction of overexpression of BAFF and B cell abnormal differentiation. The possible promotion of BAFF overexpression in the mice spleen macrophages during polarization to M1 by T3 was also studied. We showed that high levels of T3 can induce BAFF overexpression and lead to abnormal differentiation of B cells in the mice. While the overexpression of BAFF was observed across many tissue types in the mice, high levels of T3 could induce M1 macrophages polarization by IFN (interferon-gamma)-γ in the spleen of the mice, which in turn generated BAFF overexpression. Our findings provide a novel insight into the interactions between the endocrine and immune systems, as well as provide insight into the role of TH in the pathogenesis of GD.https://doi.org/10.1177/09636897231204075
spellingShingle Shu Liu
Guo-Qing Li
Qing-Wei Gu
Jie Wang
Qi Sun
Wen-Sha Gu
Xiao-Ming Mao
Induced Overexpression of B Cell-Activating Factor by Triiodothyronine Results in Abnormal B Cell Differentiation in Mice
Cell Transplantation
title Induced Overexpression of B Cell-Activating Factor by Triiodothyronine Results in Abnormal B Cell Differentiation in Mice
title_full Induced Overexpression of B Cell-Activating Factor by Triiodothyronine Results in Abnormal B Cell Differentiation in Mice
title_fullStr Induced Overexpression of B Cell-Activating Factor by Triiodothyronine Results in Abnormal B Cell Differentiation in Mice
title_full_unstemmed Induced Overexpression of B Cell-Activating Factor by Triiodothyronine Results in Abnormal B Cell Differentiation in Mice
title_short Induced Overexpression of B Cell-Activating Factor by Triiodothyronine Results in Abnormal B Cell Differentiation in Mice
title_sort induced overexpression of b cell activating factor by triiodothyronine results in abnormal b cell differentiation in mice
url https://doi.org/10.1177/09636897231204075
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