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( Henrike J Fischer ),( Jens Van Den Brandt ),( Holger M Reichardt ) 대한내과학회 2014 대한내과학회 추계학술발표논문집 Vol.2014 No.1
T cells are an important line of defense against infections. Following antigen recognition they become activated and start to express the insulin receptor (InsR), which helps to cover the cells`s increased energy demand. Here we report that full activation of T cells could not be achieved when the InsR was ablated in transgenic knock-down rats. This was refi ected by a delayed up-regulation of CD25, a reduced secretion of pro-infiammatory cytokines and a diminished proliferation of CD4+ T cells. Interestingly, the observed effects were unrelated to differences in gene expression but rather seemed to be caused by alterations at the post-transcriptional level. CD8+ T cells, which are central to the clearance of viral infections, were also affected by the absence of the InsR. In particular their cytotoxic activity against foreign antigen was signifi cantly reduced. Preliminary experiments further suggested that adaptive immune responses in vivo were dampened when the InsR was absent in T cells. Collectively, our fi ndings indicate that insulin signaling fosters T cell activation. We would therefore expect that various T cell functions are compromised in patients with type 2 diabetes mellitus, which might explain why they are at greater risk of infections.