期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 191, 期 11, 页码 2021-2027出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.191.11.2021
关键词
activation; CTL; diabetes; CD40; costimulation
The mechanisms that determine whether receptor stimulation leads to lymphocyte tolerance versus activation remain poorly understood. We have used rat insulin promoter (RIP)-gp/P14 double-transgenic mice expressing the: lymphocytic choriomeningitis virus (LCMV) glycoprotein (gp) on pancreatic beta-islet: cells together with T cells expressing an LCMV-gp-specific T cell receptor to assess the requirements for the induction of autoimmunity. Our studies have shown that administration of the gp peptide gp33 leads to the activation of P14-transgenic T cells, as measured by the upregulation of activation markers and the induction of effector cytotoxic activity. This treatment also leads to expansion and deletion of P14 T cells. Despite the induction of cytotoxic T lymphocyte activity, peptide administration is not sufficient to induce diabetes. However, the administration of gp peptide together with an activating anti-CD40 antibody rapidly induces diabetes. These findings suggest that the induction of tolerance versus autoimmunity is determined by resting versus activated antigen-presenting cells.
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