BHLHE40介导实验性自身免疫性脑脊髓炎期间致病性TH17细胞和骨髓细胞之间的串扰。

Q3 Medicine
Melissa E Cook, Irina Shchukina, Chih-Chung Lin, Tara R Bradstreet, Elizabeth A Schwarzkopf, Nicholas N Jarjour, Ashlee M Webber, Konstantin Zaitsev, Maxim N Artyomov, Brian T Edelson
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引用次数: 0

摘要

TH17细胞与多发性硬化症和实验性自身免疫性脑脊髓炎(EAE)的发病机制有关。我们之前报道了转录因子碱性螺旋-环-螺旋家族成员e40(BHLHE40)在EAE期间标记产生细胞因子的致病性TH细胞,并且其在T细胞中的表达是临床疾病所必需的。在这项研究中,使用双报告基因小鼠,我们显示了EAE诱导后BHLHE40在TH1/17和ex-TH17细胞中的表达。Il17a-Cre介导的TH细胞中BHLHE40的缺失导致不太严重的EAE,同时TH细胞因子的产生减少。通过单细胞RNA测序对EAE期间中枢神经系统中的白细胞进行表征,确定了当BHLHE40存在或不存在于TH17细胞中时,浸润性骨髓细胞中的差异。我们的研究强调了BHLHE40在促进TH17细胞的脑炎原性和指导活性EAE期间的髓细胞反应方面的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
BHLHE40 Mediates Cross-Talk between Pathogenic TH17 Cells and Myeloid Cells during Experimental Autoimmune Encephalomyelitis.

TH17 cells are implicated in the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). We previously reported that the transcription factor basic helix-loop-helix family member e40 (BHLHE40) marks cytokine-producing pathogenic TH cells during EAE, and that its expression in T cells is required for clinical disease. In this study, using dual reporter mice, we show BHLHE40 expression within TH1/17 and ex-TH17 cells following EAE induction. Il17a-Cre-mediated deletion of BHLHE40 in TH cells led to less severe EAE with reduced TH cell cytokine production. Characterization of the leukocytes in the CNS during EAE by single-cell RNA sequencing identified differences in the infiltrating myeloid cells when BHLHE40 was present or absent in TH17 cells. Our studies highlight the importance of BHLHE40 in promoting TH17 cell encephalitogenicity and instructing myeloid cell responses during active EAE.

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来源期刊
CiteScore
3.70
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