TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses.
TIM-4 Identifies Effector B Cells Expressing An IL-23-Driven Proinflammatory Cytokine Module That Promotes Immune Responses.
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TIM-4 可识别表达 IL-23 驱动的促炎细胞因子模块的效应 B 细胞，从而促进免疫反应。
DOI：
10.1101/2023.09.22.558524
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发表时间：
2023
期刊：
影响因子：
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通讯作者：
Rothstein,DavidM
中科院分区：
文献类型：
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作者：
Ding,Qing;Wu,Yufan;Triglia,ElenaTorlai;Gommerman,JenniferL;Subramanian,Ayshwarya;Kuchroo,VijayK;Rothstein,DavidM
B细胞可以表达促炎细胞因子，促进多种免疫反应。本研究表明，表达磷脂酰丝氨酸受体TIM-4的B细胞不仅优先表达IL-17A，还优先表达IL-22、IL-6和gm - csf，这是一组与致病性Th17细胞相似的细胞因子。这种促炎模块的表达需要B细胞表达IL-23R、RORγt和IL-17。TIM-4+ B细胞表达IL-17不仅能增强实验性自身免疫性脑脊髓炎（EAE）的严重程度，促进同种异体移植排斥反应，还能自分泌阻止其转化为具有调节功能的表达il -10的B细胞。因此，IL-17作为炎症介质，也增强了TIM-4+ B细胞的促炎活性。TIM-4作为效应B细胞（Beff）的广泛标记物，将允许研究调节其分化和效应分子表达的信号。
B cells can express pro-inflammatory cytokines that promote a wide variety of immune responses. Here we show that B cells expressing the phosphatidylserine receptor TIM-4, preferentially express not only IL-17A, but also IL-22, IL-6, and GM-CSF-a collection of cytokines reminiscent of pathogenic Th17 cells. Expression of this proinflammatory module requires B cell expression of IL-23R, RORγt and IL-17. IL-17 expressed by TIM-4+ B cells not only enhances the severity of experimental autoimmune encephalomyelitis (EAE) and promotes allograft rejection, but also acts in an autocrine manner to prevent their conversion into IL-10-expressing B cells with regulatory function. Thus, IL-17 acts as an inflammatory mediator and also enforces the proinflammatory activity of TIM-4+ B cells. TIM-4 serves as a broad marker for effector B cells (Beff) that will allow the study of the signals regulating their differentiation and expression of their effector molecules.