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Blood, 12 March 2009, Vol. 113, No. 11, pp. 2426-2433. Prepublished online as a Blood First Edition Paper on November 19, 2008; DOI 10.1182/blood-2008-04-154682. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-04-154682v1 113/11/2426    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Eddahri, F. Articles by Andris, F. Search for Related Content PubMed PubMed Citation Articles by Eddahri, F. Articles by Andris, F. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 29, 2008 Accepted November 14, 2008 Interleukin-6 / STAT3 signalling regulates the ability of naive T cells to acquire B cell help capacities Fouad Eddahri, Sebastien Denanglaire, Fabrice Bureau, Rosanne Spolski, Warren J Leonard, Oberdan Leo, and Fabienne Andris* Laboratoire de Physiologie Animale, Universite Libre de Bruxelles, Gosselies, Belgium Laboratory of Cellular and Molecular Physiology, GIGA-Research, University of Liege, Liege, Belgium Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD, United States * Corresponding author; email: fandris{at}ulb.ac.be. The conditions leading to the activation / differentiation of T helper (Th) cells dedicated for B cell antibody production are still poorly characterized. We now demonstrate that interleukin (IL)-6 promotes the differentiation of naive T lymphocytes into helper cells able to promote B cell activation and antibody secretion. IL-6 driven- acquisition of B cell help capacity requires expression of the STAT3, but not STAT4 or STAT6 transcription factors, suggesting that the ability to provide help to B cells is not restricted to a well-defined Th1 or Th2 effector population. T-cell specific STAT3-deficient mice displayed reduced humoral responses in vivo that could not be related to an altered expansion of CXCR5-expressing helper T cells. IL-6 was shown to promote IL-21 secretion, a cytokine that was similarly found to promote the differentiation of naive T cells into potent B cell helper cells. Collectively these data indicate that the ability to provide B cell help is regulated by IL-6 / IL-21 through STAT3 activation, independently of Th1, Th2, Th17 or TFH differentiation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Spolski and W. J. Leonard IL-21 and T follicular helper cells Int. Immunol., November 23, 2009; (2009) dxp112v1. [Abstract] [Full Text] [PDF] A. M. Didierlaurent, S. Morel, L. Lockman, S. L. Giannini, M. Bisteau, H. Carlsen, A. Kielland, O. Vosters, N. Vanderheyde, F. Schiavetti, et al. AS04, an Aluminum Salt- and TLR4 Agonist-Based Adjuvant System, Induces a Transient Localized Innate Immune Response Leading to Enhanced Adaptive Immunity J. Immunol., November 15, 2009; 183(10): 6186 - 6197. [Abstract] [Full Text] [PDF]

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