A key role for ICAM-I in generating effector cells mediating inflammatory responses

Abstract

We investigated how the accessory molecule interactions encountered during T cell priming influence T cell-mediated destruction of insulin-producing β cells and lead to type I 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 I (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 prime..