TRIF Mediates Toll-Like Receptor 2-Dependent Inflammatory Responses to Borrelia burgdorferi

• DOI: 10.1128/iai.00890-12
• Publication Date: 2012-11-20T04:54:31Z
• Authors: Tanja Petnicki-Oc...; Erin Chung; David I. Acosta; Laurie T. Ramos; Ok S. Shin; Sanjukta Ghosh; Lester Kobzik; Xin Li; Linden T. Hu
• Keywords: TRIF; TLR3

ABSTRACT TRIF is an adaptor molecule important in transducing signals from intracellularly signaling Toll-like receptor 3 (TLR3) and TLR4. Recently, TLR2 was found to signal intracellular compartments. Using a synthetic ligand for TLR2/1 heterodimers, as well Borrelia burgdorferi , which strong activator of TLR2/1, we that can utilize TRIF. Unlike by other TLRs, TLR2-mediated dependent on the presence another molecule, MyD88. However, unlike MyD88 deficiency, deficiency does not result diminished control infection with B. murine model disease. This appears be due effects phagocytosis via scavenger receptors, such MARCO, are affected loss In mice, did have effect production inflammatory cytokines, suggesting regulation cytokines bacterial growth may uncoupled, part through transduction