| First Author | Moser B | Year | 2007 |
| Journal | J Immunol | Volume | 179 |
| Issue | 12 | Pages | 8051-8 |
| PubMed ID | 18056345 | Mgi Jnum | J:155203 |
| Mgi Id | MGI:4412453 | Doi | 10.4049/jimmunol.179.12.8051 |
| Citation | Moser B, et al. (2007) Receptor for advanced glycation end products expression on T cells contributes to antigen-specific cellular expansion in vivo. J Immunol 179(12):8051-8 |
| abstractText | 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-gamma 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. |
