Attenuation of CD4+ T-cell function by human adenovirus type 35 is mediated by the knob protein.

作者: William C. Adams , Ronald J. Berenson , Gunilla B. Karlsson Hedestam , André Lieber , Richard A. Koup

DOI: 10.1099/VIR.0.039222-0

关键词: CD46Acquired immune systemIn vitroMutantRecombinant DNAMolecular biologyBiologyVirus geneticsVirologyReceptorDownregulation 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.

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