作者: Danny Zipris , Jan-Luuk Hillebrands , Raymond M. Welsh , Jan Rozing , Jenny X. Xie
DOI: 10.4049/JIMMUNOL.170.7.3592
关键词:
摘要: Viruses are believed to contribute the pathogenesis of autoimmune type 1A diabetes in humans. This pathogenic process can be modeled BBDR rat, which develops pancreatic insulitis and 1A-like after infection with Kilham's rat virus (RV). The mechanism is unknown, but does not involve islets. We first documented that RV rats induces diabetes, whereas its close homologue H-1 not. Both viruses induced similar humoral cellular immune responses host, only also caused a decrease splenic CD4(+)CD25(+) T cells both normal WF rats. Surprisingly, increased lymph nodes increase appeared due accumulation nonproliferating cells. results imply reduction observed RV-infected animals specific, node strain specific. data suggest alters cell regulation permits expression diabetes. More generally, could link an underlying genetic predisposition environmental perturbation transform "regulated predisposition" into namely, failure maintain regulatory function.