title: Recognition of microbial infection by Toll-like receptors.
abstract: The Toll-like receptors (TLRs) of the innate immune system detect host invasion by pathogens and initiate immune responses. All of the TLRs use the adaptor MyD88 to transduce a signal; however, two newly identified signaling molecules, TIRAP and TRIF, interact with a subset of the TLRs, suggesting a signaling specificity that may be relevant to the type of infection. Activation of the TRIF pathway, for example, leads to the production of antiviral gene products via the transcription factor, IRF3. In vivo experiments in TLR-deficient mice underscore the importance of TLRs in overcoming infection.
authors.affiliation: Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Kopp
authors.forename: Ruslan
authors.initials: R
authors.lastname: Medzhitov
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D000943:Antigens, Differentiation / Q000378:metabolism; D006801:Humans; D007239:Infections / Q000276:immunology* / Q000382:microbiology*; D008562:Membrane Glycoproteins / Q000276:immunology*; D053594:Myeloid Differentiation Factor 88; D011956:Receptors, Cell Surface / Q000276:immunology*; D011971:Receptors, Immunologic / Q000378:metabolism; D015398:Signal Transduction; D051193:Toll-Like Receptors
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D000943:Antigens, Differentiation; C507779:MYD88 protein, human; D008562:Membrane Glycoproteins; D053594:Myeloid Differentiation Factor 88; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; D051193:Toll-Like Receptors