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c-Myb Regulates the T-Bet-Dependent Differentiation Program in B Cells to Coordinate Antibody Responses.

Abstract：

:Humoral immune responses are tailored to the invading pathogen through regulation of key transcription factors and their networks. This is critical to establishing effective antibody-mediated responses, yet it is unknown how B cells integrate pathogen-induced signals to drive or suppress transcriptional programs specialized for each class of pathogen. Here, we detail the key role of the transcription factor c-Myb in regulating the T-bet-mediated anti-viral program. Deletion of c-Myb in mature B cells significantly increased serum IgG2c and CXCR3 expression by upregulating T-bet, normally suppressed during Th2-cell-mediated responses. Enhanced expression of T-bet resulted in aberrant plasma cell differentiation within the germinal center, mediated by CXCR3 expression. These findings identify a dual role for c-Myb in limiting inappropriate effector responses while coordinating plasma cell differentiation with germinal center egress. Identifying such intrinsic regulators of specialized antibody responses can assist in vaccine design and therapeutic intervention in B-cell-mediated immune disorders.

journal_name

Cell Rep

journal_title

Cell reports

authors

Piovesan D,Tempany J,Di Pietro A,Baas I,Yiannis C,O'Donnell K,Chen Y,Peperzak V,Belz GT,Mackay CR,Smyth GK,Groom JR,Tarlinton DM,Good-Jacobson KL

doi

10.1016/j.celrep.2017.03.060

subject

Has Abstract

pub_date

2017-04-18 00:00:00

pages

461-470

issue

3

issn

2211-1247

pii

S2211-1247(17)30421-7

journal_volume

19

pub_type

杂志文章

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