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Sci Immunol. 2017 Oct 20;2(16). pii: eaan4767. doi: 10.1126/sciimmunol.aan4767.

Interleukin-10 from CD4+ follicular regulatory T cells promotes the germinal center response.

Author information

1
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
2
Department of Internal Medicine (Rheumatology), Yale University School of Medicine, New Haven, CT 06520, USA.
3
Interdepartmental Program in Computational Biology and Bioinformatics, Yale University School of Medicine, New Haven, CT 06520, USA.
4
Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.
5
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. joseph.craft@yale.edu.

Abstract

CD4+ follicular regulatory T (Tfr) cells suppress B cell responses through modulation of follicular helper T (Tfh) cells and germinal center (GC) development. We found that Tfr cells can also promote the GC response through provision of interleukin-10 (IL-10) after acute infection with lymphocytic choriomeningitis virus (LCMV). Sensing of IL-10 by B cells was necessary for optimal development of the GC response. GC B cells formed in the absence of Treg cell-derived IL-10 displayed an altered dark zone state and decreased expression of the transcription factor Forkhead box protein 1 (FOXO1). IL-10 promoted nuclear translocation of FOXO1 in activated B cells. These data indicate that Tfr cells play a multifaceted role in the fine-tuning of the GC response and identify IL-10 as an important mediator by which Tfr cells support the GC reaction.

PMID:
29054998
PMCID:
PMC5846620
DOI:
10.1126/sciimmunol.aan4767
[Indexed for MEDLINE]
Free PMC Article

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