作者: William C. Adams , Ronald J. Berenson , Gunilla B. Karlsson Hedestam , André Lieber , Richard A. Koup
关键词: CD46 、 Acquired immune system 、 In vitro 、 Mutant 、 Recombinant DNA 、 Molecular biology 、 Biology 、 Virus genetics 、 Virology 、 Receptor 、 Downregulation and upregulation
摘要: The complement-regulatory protein CD46 is the primary receptor for human adenovirus type 35 (HAdV-35) and can regulate immune-cell activation. CD4(+) T-cells are critical initiating maintaining adaptive immunity elicited by infection or vaccination. It was reported previously that HAdV-35 bind these cells suppress their data here demonstrate recombinant trimeric knob proteins alone induce downregulation inhibit interleukin-2 production proliferation of in vitro similarly to mAbs specific region bound knobs. A mutant with increased affinity compared wild-type caused equivalent effects. In contrast, a CD46-binding-deficient did not T-cell Thus, capacity attenuate activation depends predominantly on interactions occur independently infection.