Journal article

IL-21 regulates germinal center B cell differentiation and proliferation through a B cell-intrinsic mechanism

Dimitra Zotos, Jonathan M Coquet, Yang Zhang, Amanda Light, Kathy D'Costa, Axel Kallies, Lynn M Corcoran, Dale I Godfrey, Kai-Michael Toellner, Mark J Smyth, Stephen L Nutt, David M Tarlinton

Journal of Experimental Medicine | ROCKEFELLER UNIV PRESS | Published : 2010

Abstract

Germinal centers (GCs) are sites of B cell proliferation, somatic hypermutation, and selection of variants with improved affinity for antigen. Long-lived memory B cells and plasma cells are also generated in GCs, although how B cell differentiation in GCs is regulated is unclear. IL-21, secreted by T follicular helper cells, is important for adaptive immune responses, although there are conflicting reports on its target cells and mode of action in vivo. We show that the absence of IL-21 signaling profoundly affects the B cell response to protein antigen, reducing splenic and bone marrow plasma cell formation and GC persistence and function, influencing their proliferation, transition into me..

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Grants

Awarded by National Health and Medical Research Council (NHMRC) Australia


Awarded by Medical Research Council


Funding Acknowledgements

This work was supported by grants from the National Health and Medical Research Council (NHMRC) Australia (454569 to M. J. Smyth and D. I. Godfrey; 356202 to D. M. Tarlinton, L. M. Corcoran, and S. L. Nutt). D. M. Tarlinton, L. M. Corcoran, M. J. Smyth, and D. I. Godfrey are supported by fellowships from the NHMRC while S. L. Nutt is supported by a Pfizer Australia Research Fellowship. D. Zotos is the recipient of an Australian Postgraduate Research Award. Y. Zhang and K. M. Toellner are supported by the European Union within the NEST project MAMOCELL.