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TIM-4 Identifies Effector B Cells Expressing a RORγt-Driven Proinflammatory Cytokine Module That Promotes Immune

Qing Ding1, Yufan Wu2, Elena Torlai Triglia2

  • 1Thomas E. Starzl Transplantation Institute; University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

Biorxiv : the Preprint Server for Biology
|October 4, 2023
PubMed

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 IL-17A, as well as IL-22, IL-6, IL-1β, and GM-CSF - a collection of cytokines reminiscent of pathogenic Th17 cells. Expression of this proinflammatory module requires IL-23R signaling and selective expression of RORγt and IL-17A by TIM-4+ B cells. TIM-4+ B cell-derived-IL-17A 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-17A acts as an inflammatory mediator and also enforces the proinflammatory activity of TIM-4+ B cells. Thus, TIM-4 serves as a broad marker for RORγt+ effector B cells (Beff) and allows further study of the signals regulating Beff differentiation and effector molecule expression.

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