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B-cell-intrinsic STAT6 signaling controls germinal center formation

Item Type:Article
Title:B-cell-intrinsic STAT6 signaling controls germinal center formation
Creators Name:Turqueti-Neves, A., Otte, M., da Costa, O.P., Höpken, U.E., Lipp, M., Buch, T. and Voehringer, D.
Abstract:Infection with helminths and exposure to antigens induce a strong type 2 immune response resulting in the secretion of the cytokines IL-4 and IL-13 by CD4(+) T cells and several innate cell types. IL-4 and IL-13 promote class switch recombination to IgG1 and IgE while their role for germinal center (GC) formation is poorly understood. We found a dramatic reduction in the numbers of GC B cells when investigating different type 2 immune responses in IL-4/IL-13-deficient mice. IL-4/IL-13 from T cells located outside B-cell follicles was sufficient for GC formation. We further revealed that IL-4/IL-13 acts directly on B cells for the formation of a robust GC response. The frequency of apoptotic GC B cells was not altered in the absence of IL-4/IL-13 and proliferation was even enhanced. However, deficiency of STAT6 signaling in B cells resulted in failure to downregulate the chemotactic receptor Gpr183 (Ebi2) and downregulation of this receptor has been shown to be essential for proper GC B cell differentiation. Thus, T cell derived extrafollicular IL-4/IL-13 and STAT6-regulated genes in B cells play a critical role for orchestration of the GC response in type 2 immunity.
Keywords:B Cells, Germinal Center, IL-4, IL-13, STAT6, Animals, Mice
Source:European Journal of Immunology
Page Range:2130-2138
Date:July 2014
Official Publication:https://doi.org/10.1002/eji.201344203
PubMed:View item in PubMed

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