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Blood, 15 May 2007, Vol. 109, No. 10, pp. 4360-4367. Prepublished online as a Blood First Edition Paper on January 16, 2007; DOI 10.1182/blood-2006-11-056424. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2006-11-056424v1 109/10/4360    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 Chen, M. Articles by Wang, J. Search for Related Content PubMed PubMed Citation Articles by Chen, M. Articles by Wang, J. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Deficiency of Bim in dendritic cells contributes to overactivation of lymphocytes and autoimmunity Min Chen1, Li Huang1, and Jin Wang1 1 Department of Immunology, Baylor College of Medicine, Houston, TX Apoptosis in dendritic cells (DCs) can potentially regulate DC homeostasis and immune responses. We have previously observed that inhibition of the Fas signaling pathway in DCs results in spontaneous T-cell activation and the development of systemic autoimmunity in transgenic mice. However, the role for different apoptosis pathways in DCs in regulating DC homeostasis and immune tolerance remains to be determined. Bim, a BH3-only protein of the Bcl-2 family, was expressed at low levels in DCs and was significantly up-regulated by signaling from CD40 or toll-like receptors (TLRs). Because Bim–/– mice develop spontaneous systemic autoimmunity, we investigated whether Bim–/– DCs contributed to lymphoproliferation and autoimmunity in these mice. Bim–/– DCs showed decreased spontaneous cell death, and induced more robust T-cell activation in vitro and in vivo. Moreover, Bim–/– DCs induced autoantibody production after adoptive transfer. Our data suggest that Bim is important for regulating spontaneous cell death in DCs, and Bim-deficient DCs may contribute to the development of autoimmune diseases in Bim–/– mice. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Escribano, C. Delgado-Martin, and J. L. Rodriguez-Fernandez CCR7-Dependent Stimulation of Survival in Dendritic Cells Involves Inhibition of GSK3{beta} J. Immunol., November 15, 2009; 183(10): 6282 - 6295. [Abstract] [Full Text] [PDF] T. Chino, K. E. Draves, and E. A. Clark Regulation of dendritic cell survival and cytokine production by osteoprotegerin J. Leukoc. Biol., October 1, 2009; 86(4): 933 - 940. [Abstract] [Full Text] [PDF] E. L. Gautier, T. Huby, F. Saint-Charles, B. Ouzilleau, J. Pirault, V. Deswaerte, F. Ginhoux, E. R. Miller, J. L. Witztum, M. J. Chapman, et al. Conventional Dendritic Cells at the Crossroads Between Immunity and Cholesterol Homeostasis in Atherosclerosis Circulation, May 5, 2009; 119(17): 2367 - 2375. [Abstract] [Full Text] [PDF] B. K. Choi, Y. H. Kim, P. M. Kwon, S. C. Lee, S. W. Kang, M. S. Kim, M. J. Lee, and B. S. Kwon 4-1BB Functions As a Survival Factor in Dendritic Cells J. Immunol., April 1, 2009; 182(7): 4107 - 4115. [Abstract] [Full Text] [PDF] M. Sundquist and M. J. Wick Salmonella induces death of CD8{alpha}+ dendritic cells but not CD11cintCD11b+ inflammatory cells in vivo via MyD88 and TNFR1 J. Leukoc. Biol., February 1, 2009; 85(2): 225 - 234. [Abstract] [Full Text] [PDF] A. Couzinet, K. Tamura, H.-m. Chen, K. Nishimura, Z. Wang, Y. Morishita, K. Takeda, H. Yagita, H. Yanai, T. Taniguchi, et al. A cell-type-specific requirement for IFN regulatory factor 5 (IRF5) in Fas-induced apoptosis PNAS, February 19, 2008; 105(7): 2556 - 2561. [Abstract] [Full Text] [PDF]

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