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Blood, 15 January 2006, Vol. 107, No. 2, pp. 594-601. Prepublished online as a Blood First Edition Paper on September 29, 2005; DOI 10.1182/blood-2004-12-4708. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-12-4708v1 107/2/594    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 Diaz-de-Durana, Y. Articles by Franco, A. Search for Related Content PubMed PubMed Citation Articles by Diaz-de-Durana, Y. Articles by Franco, A. Related Collections Signal Transduction Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY TACI-BLyS signaling via B-cell–dendritic cell cooperation is required for naive CD8+ T-cell priming in vivo Yaiza Diaz-de-Durana, George T. Mantchev, Richard J. Bram, and Alessandra Franco From the Torrey Pines Institute for Molecular Studies, San Diego, CA; the University of California–San Diego; and the Mayo Clinic and Foundation, Rochester, MN. We demonstrated that B-cell–dendritic cell (DC) interactions via transmembrane activator and calcium modulator and cyclophilin ligand (CAML) interactor (TACI) and B-lymphocyte stimulator (BLyS) provide an early signal critical to generate adequate numbers of mature antigen presenting cells (APCs) to prime naive CD8+ T cells (CTLs) in vivo. Evidence that B cells are required for efficient CTL generation in mice and that reconstitution with wild-type but not TACI-knockout B cells restored normal CTL responses support our conclusion. Moreover, low doses of a TACI fusion protein (TACI-Fc) that express the extracellular domain of TACI (amino acid [aa] 1-126) restored CTL priming in B-cell–deficient mice in vivo and induced DC maturation in vitro. In fact, following interactions with B cells, splenic DCs rapidly express the CD86 costimulatory molecule, to an extent comparable to the exposure to antigenic stimuli. BLyShigh peptide-pulsed bone marrow–derived DCs, used as vaccines in vivo, cannot generate CTLs in B-cell–deficient and TACI-deficient mice, strongly supporting a need for B-cell–DC cooperation through TACI-BLyS during CTL first encounter with antigens in vivo. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Fehr, F. Haspot, J. Mollov, M. Chittenden, T. Hogan, and M. Sykes Alloreactive CD8 T Cell Tolerance Requires Recipient B Cells, Dendritic Cells, and MHC Class II J. Immunol., July 1, 2008; 181(1): 165 - 173. [Abstract] [Full Text] [PDF] G. M. Brodie, M. Wallberg, P. Santamaria, F. S. Wong, and E. A. Green B-Cells Promote Intra-Islet CD8+ Cytotoxic T-Cell Survival to Enhance Type 1 Diabetes Diabetes, April 1, 2008; 57(4): 909 - 917. [Abstract] [Full Text] [PDF] S. Sarantopoulos, K. E. Stevenson, H. T. Kim, N. S. Bhuiya, C. S. Cutler, R. J. Soiffer, J. H. Antin, and J. Ritz High Levels of B-Cell Activating Factor in Patients with Active Chronic Graft-Versus-Host Disease Clin. Cancer Res., October 15, 2007; 13(20): 6107 - 6114. [Abstract] [Full Text] [PDF] Q. Liu, Z. Liu, C. T. Rozo, H. A. Hamed, F. Alem, J. F. Urban Jr., and W. C. Gause The Role of B Cells in the Development of CD4 Effector T Cells during a Polarized Th2 Immune Response J. Immunol., September 15, 2007; 179(6): 3821 - 3830. [Abstract] [Full Text] [PDF]

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