| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
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.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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.
Related articles in The JI:
This article has been cited by other articles:
|
|
 |
|
  T. Watanabe, H. Keino, Y. Sato, A. Kudo, H. Kawakami, and A. A. Okada High Mobility Group Box Protein-1 in Experimental Autoimmune Uveoretinitis Invest. Ophthalmol. Vis. Sci., May 1, 2009; 50(5): 2283 - 2290. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Chen, E. M. Akirav, W. Chen, O. Henegariu, B. Moser, D. Desai, J. M. Shen, J. C. Webster, R. C. Andrews, A. M. Mjalli, et al. RAGE Ligation Affects T Cell Activation and Controls T Cell Differentiation J. Immunol., September 15, 2008; 181(6): 4272 - 4278. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Ramasamy, S. F. Yan, and A. M. Schmidt Stopping the Primal RAGE Reaction in Myocardial Infarction: Capturing Adaptive Responses to Heal the Heart? Circulation, June 24, 2008; 117(25): 3165 - 3167. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
