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CD5 Binds to Interleukin-6 and Induces a Feed-Forward Loop with the Transcription Factor STAT3 in B Cells to Promote Cancer.

Abstract：

:The participation of a specific subset of B cells and how they are regulated in cancer is unclear. Here, we demonstrate that the proportion of CD5(+) relative to interleukin-6 receptor α (IL-6Rα)-expressing B cells was greatly increased in tumors. CD5(+) B cells responded to IL-6 in the absence of IL-6Rα. IL-6 directly bound to CD5, leading to activation of the transcription factor STAT3 via gp130 and its downstream kinase JAK2. STAT3 upregulated CD5 expression, thereby forming a feed-forward loop in the B cells. In mouse tumor models, CD5(+) but not CD5(-) B cells promoted tumor growth. CD5(+) B cells also showed activation of STAT3 in multiple types of human tumor tissues. Thus, our findings demonstrate a critical role of CD5(+) B cells in promoting cancer.

journal_name

Immunity

journal_title

Immunity

authors

Zhang C,Xin H,Zhang W,Yazaki PJ,Zhang Z,Le K,Li W,Lee H,Kwak L,Forman S,Jove R,Yu H

doi

10.1016/j.immuni.2016.04.003

subject

Has Abstract

pub_date

2016-04-19 00:00:00

pages

913-923

issue

4

eissn

1074-7613

issn

1097-4180

journal_volume

44

pub_type

杂志文章

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