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Publication : Efficient T cell activation via a Toll-Interleukin 1 Receptor-independent pathway.

First Author  Janssen E Year  2006
Journal  Immunity Volume  24
Issue  6 Pages  787-99
PubMed ID  16782034 Mgi Jnum  J:113369
Mgi Id  MGI:3665523 Doi  10.1016/j.immuni.2006.03.024
Citation  Janssen E, et al. (2006) Efficient T cell activation via a Toll-Interleukin 1 Receptor-independent pathway. Immunity 24(6):787-99
abstractText  Here, we describe a previously unrecognized pathway for activation of antigen-specific adaptive immune responses that was independent of Toll-Interleukin 1 Receptor signaling and directed toward detection of antigens expressed by apoptotic cells. This pathway is represented within Flt-3 Ligand-derived dendritic cells (DCs) that represent immature lymphoid DCs, but not within GM-CSF-treated bone marrow-derived dendritic cells. Exposure of these DCs to apoptotic cells resulted in production of type I interferon and favored the development of cytotoxic T cell responses. The N-Ethyl-N-Nitrosourea-induced germline mutation 3d (Unc3b1(3d/3d)) abolished both MHC class I and II responses elicited by this pathway, whereas a null allele of Cd36 selectively abolished class II responses. We propose that this mode of adaptive immune activation evolved to permit the sensitive detection of intracellular microbial infections, particularly viral infections, which frequently induce apoptotic cell death, but may also be important in transplantation, autoimmunity, and vaccine development.
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