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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 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 Citation Map 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. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Interleukin-6/STAT3 signaling regulates the ability of naive T cells to acquire B-cell help capacities Fouad Eddahri1, Sébastien Denanglaire1, Fabrice Bureau2, Rosanne Spolski3, Warren J. Leonard3, Oberdan Leo1,*, and Fabienne Andris1,* 1 Laboratoire de Physiologie Animale, Université Libre de Bruxelles, Bruxelles, Belgium; 2 Laboratory of Cellular and Molecular Physiology, Groupe Interdisciplinaire de Génomique Appliquée–Research, University of Liège, Liège, Belgium; and 3 Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 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-6 (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 signal transducer and activator of transcription 3 (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 follicular helper T cell (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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