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The Transcription Factor AP4 Mediates Resolution of Chronic Viral Infection through Amplification of Germinal Center B Cell Responses.

Abstract：

:B cells diversify and affinity mature their antigen receptor repertoire in germinal centers (GCs). GC B cells receive help signals during transient interaction with T cells, yet it remains unknown how these transient T-B interactions in the light zone sustain the subsequent proliferative program of selected B cells that occurs in the anatomically distant dark zone. Here, we show that the transcription factor AP4 was required for sustained GC B cell proliferation and subsequent establishment of a diverse and protective antibody repertoire. AP4 was induced by c-MYC during the T-B interactions, was maintained by T-cell-derived interleukin-21 (IL-21), and promoted repeated rounds of divisions of selected GC B cells. B-cell-specific deletion of AP4 resulted in reduced GC sizes and reduced somatic hypermutation coupled with a failure to control chronic viral infection. These results indicate that AP4 integrates T-cell-mediated selection and sustained expansion of GC B cells for humoral immunity.

journal_name

Immunity

journal_title

Immunity

authors

Chou C,Verbaro DJ,Tonc E,Holmgren M,Cella M,Colonna M,Bhattacharya D,Egawa T

doi

10.1016/j.immuni.2016.07.023

subject

Has Abstract

pub_date

2016-09-20 00:00:00

pages

570-582

issue

3

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(16)30296-5

journal_volume

45

pub_type

杂志文章

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