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Dexamethasone reduces autoantibody levels in MRL/lpr mice by inhibiting Tfh cell responses
Author(s) -
Shen Chunxiu,
Xue Xiaonan,
Zhang Xiaoyu,
Wu Lihua,
Duan Xiangguo,
Su Chunxia
Publication year - 2021
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16785
Subject(s) - cxcr5 , germinal center , follicular phase , dexamethasone , endocrinology , medicine , messenger rna , antibody , b cell , autoantibody , chemistry , biology , immunology , gene , biochemistry
Previous studies have shown that dexamethasone (Dex) reduces the levels of anti‐nuclear (ANA) and anti‐dsDNA antibodies in MRL/lpr mice (a mouse model of SLE). However, the effect of Dex on T follicular helper (Tfh) cells is less documented. Here, using the MRL/lpr mouse model, we investigated the influence of Dex on Tfh cells and potential underlying mechanisms. The data showed that the proportion of Tfh cells, identified as CD4 + CXCR5 + ICOS + , CD4 + CXCR5 + PD‐1 + or CD4 + BCL‐6 + cells, markedly decreased after treatment with the Dex, in both Balb/c mice and MRL/lpr mice. Dex significantly inhibited IL‐21 expression at both the mRNA and the protein levels. Dex also significantly reduced the proportion of germinal centre B cells and decreased serum IgG, IgG2a/b and IgA levels. Moreover, a positive correlation between the proportion of Tfh cells (CD4 + CXCR5 + ICOS + , CD4 + CXCR5 + PD‐1 + or CD4 + BCL‐6 + ) and autoantibodies was observed. Dex significantly increased the Prdm1 and Stat5b mRNA expression and decreased the Bcl‐6 and c‐Maf mRNA expression of CD4 + T cells. In brief, Dex inhibited the Tfh development, which relies on many other transcription factors in addition to Bcl‐6 . Our data indicate that Dex can be used as a Tfh cell inhibitor in SLE.

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