The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20081571
The Journal of Experimental Medicine, Vol. 206, No. 1, 69-78
The Rockefeller University Press, 0022-1007 $30.00
© Dienz et al.
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BRIEF DEFINITIVE REPORT

 The induction of antibody production by IL-6 is indirectly mediated by IL-21 produced by CD4+ T cells

Oliver Dienz1, Sheri M. Eaton3, Jeffrey P. Bond2, Wendy Neveu1, David Moquin1, Rajkumar Noubade1, Eva M. Briso1, Colette Charland1, Warren J. Leonard4, Gennaro Ciliberto5, Cory Teuscher1, Laura Haynes3, and Mercedes Rincon1

1 Department of Medicine/Immunobiology Program and 2 Department of Microbiology and Molecular Genetics/Bioinformatics, University of Vermont, Burlington, VT 05405
3 Trudeau Institute, Saranac Lake, NY 12983
4 Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892
5 Istituto di Ricerche di Biologia Molecolare P. Angeletti, 00040 Pomezia, Roma, Italy

CORRESPONDENCE Mercedes Rincon: mrincon{at}uvm.edu

Interleukin (IL) 6 is a proinflammtory cytokine produced by antigen-presenting cells and nonhematopoietic cells in response to external stimuli. It was initially identified as a B cell growth factor and inducer of plasma cell differentiation in vitro and plays an important role in antibody production and class switching in vivo. However, it is not clear whether IL-6 directly affects B cells or acts through other mechanisms. We show that IL-6 is sufficient and necessary to induce IL-21 production by naive and memory CD4+ T cells upon T cell receptor stimulation. IL-21 production by CD4+ T cells is required for IL-6 to promote B cell antibody production in vitro. Moreover, administration of IL-6 with inactive influenza virus enhances virus-specific antibody production, and importantly, this effect is dependent on IL-21. Thus, IL-6 promotes antibody production by promoting the B cell helper capabilities of CD4+ T cells through increased IL-21 production. IL-6 could therefore be a potential coadjuvant to enhance humoral immunity.

© 2009 Dienz et al.
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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