| First Author | Camacho SA | Year | 2001 |
| Journal | Nat Immunol | Volume | 2 |
| Issue | 6 | Pages | 523-9 |
| PubMed ID | 11376339 | Mgi Jnum | J:69808 |
| Mgi Id | MGI:2135490 | Doi | 10.1038/88720 |
| Citation | Camacho SA, et al. (2001) A key role for ICAM-1 in generating effector cells mediating inflammatory responses. Nat Immunol 2(6):523-9 |
| abstractText | We investigated how the accessory molecule interactions encountered during T cell priming influence T cell-mediated destruction of insulin-producing beta cells and lead to type 1 diabetes. T cell receptor (TCR)-transgenic CD4+ T cells were primed under controlled conditions in vitro before being adoptively transferred into transgenic recipients expressing membrane ovalbumin under the control of the rat insulin promoter (RIP-mOVA). During priming, antigen-presenting cell expression of B7-1 without intracellular adhesion molecule 1 (ICAM-1) led to the generation of effector cells that migrated to the pancreata of RIP-mOVA recipients but did not cause diabetes. In contrast, when T cells were primed with APCs expressing both B7-1 and ICAM-1, pronounced destruction of beta cells and a rapid onset of diabetes were observed. Pathogenicity was associated with T cell production of the macrophage-attracting chemokines CCL3 and CCL4. Thus, interactions of lymphocyte function-associated antigen 1 with ICAM-1 during priming induce both qualitative and quantitative alterations in T effector function and induce potentially autodestructive responses. |
