Abstract

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-me-diated 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. Toll-like receptors (TLRs) are germline-encoded innate im-mune sensors of microbial pathogens [1]. Activation of TLR signaling results in induction of proinflammatory cytokines and antimicrobial peptides [1]. Experimental observations suggest that TLR2 is involved in the innate immune response to cy-tomegalovirus (CMV) [2, 3]. Stimulation of TLR2 by CMV in vitro, specifically by its envelope glycoproteins B (gB) and H