The R753Q Polymorphism Abrogates Toll‐Like Receptor 2 Signaling in Response to Human Cytomegalovirus | Zendy

Robert A. Brown | Zendy; Jonathon H. Gralewski | Zendy; Raymund R. Razonable | Zendy

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The R753Q Polymorphism Abrogates Toll‐Like Receptor 2 Signaling in Response to Human Cytomegalovirus

Author(s) -

Robert A. Brown,

Jonathon H. Gralewski,

Raymund R. Razonable

Publication year - 2009

Publication title -

clinical infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.44

H-Index - 336

eISSN - 1537-6591

pISSN - 1058-4838

DOI - 10.1086/644501

Subject(s) - tlr2 , toll like receptor , immunology , receptor , human cytomegalovirus , immune system , cytomegalovirus , medicine , signal transduction , polymorphism (computer science) , virology , innate immune system , biology , herpesviridae , virus , gene , genetics , genotype , viral disease

Toll-like receptor 2 (TLR2) serves as a pattern recognition receptor that signals the presence of cytomegalovirus. Herein, we report that R753Q polymorphism paralyzes TLR2-mediated immune signaling in cells exposed to cytomegalovirus glycoprotein B. This immunologic impairment could serve as a biologic mechanism underlying the association between the TLR2 R753Q polymorphism and cytomegalovirus disease in humans.

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