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Departments of
* Medicine, and Microbiology, and
Surgery, Columbia University College of Physicians and Surgeons, New York, NY 10032; and
Department of Immunobiology, Yale University, New Haven, CT 06520
Receptor for advanced glycation end products (RAGE) is an activation receptor triggered by inflammatory S100/calgranulins and high mobility group box-1 ligands. We have investigated the importance of RAGE on Ag priming of T cells in murine models in vivo. RAGE is inducibly up-regulated during T cell activation. Transfer of RAGE-deficient OT II T cells into OVA-immunized hosts resulted in reduced proliferative responses that were further diminished in RAGE-deficient recipients. Examination of RAGE-deficient dendritic cells did not reveal functional impairment in Ag presentation, maturation, or migratory capacities. However, RAGE-deficient T cells showed markedly impaired proliferative responses in vitro to nominal and alloantigens, in parallel with decreased production of IFN-
and IL-2. These data indicate that RAGE expressed on T cells is required for efficient priming of T cells and elucidate critical roles for RAGE engagement during cognate dendritic cell-T cell interactions.
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1 This work was supported by the Juvenile Diabetes Research Foundation.
2 B.M. and D.D.D. contributed equally to this work.
3 Address correspondence and reprint requests to Dr. Raphael Clynes, Columbia University, P and S Building, Room 8-510, 630 West 168th Street, New York, NY 10032. E-mail address: rc645{at}columbia.edu
4 Abbreviations used in this paper: RAGE, receptor for advanced glycation end products; HMGB-1, nuclear protein high mobility group box 1; sRAGE, soluble RAGE; poly(I:C), polyinosinic-polycytidylic acid; DTH, delayed-type hypersensitivity; DC, dendritic cell; Flt3L, fms-like tyrosine kinase-3 ligand; BMDC, bone marrow DC; 5(6)-TRITC, tetramethylrhodamine-5-(and -6)isothiocyanate; pDC, plasmacytoid DC; cDC, conventional DC.
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