Toll-like receptors: sentinels of host defence against bacterial infection.
Innate immunity provides a first line of host defence against infection through microbial recognition and killing while simultaneously activating a definitive adaptive immune response. Toll-like receptors (TLRs) are principal mediators of rapid microbial recognition and function mainly by detection of structural patterns that do not exist in the host. TLR2 and TLR4 were the first members of this innate immune receptor family to be strongly implicated in antibacterial host defence. Following the initial description of the mammalian TLR family, susceptibility to infection with numerous human microbial pathogens has been intensively studied using mice with engineered deletions of each of these molecules. While it has become quite clear that TLR activation is necessary for optimal host defence, a comprehensive understanding of the mechanisms by which this family of pattern recognition receptors engages protective immunity, particularly the adaptive response, is still evolving.
Schnare
Markus
M
Institute for Clinical Microbiology, Immunology and Hygiene, University of Erlangen-Nuremberg, Erlangen, Germany. markus.schnare@mikrobio.med.uni-erlangen.de
Rollinghoff
Martin
M
Qureshi
Salman
S
D048868:Adaptor Proteins, Signal Transducing / Q000276:immunology; D000818:Animals; D000943:Antigens, Differentiation / Q000276:immunology; D001424:Bacterial Infections / Q000276:immunology*; D006801:Humans; D007110:Immunity, Active; D007113:Immunity, Innate; D053594:Myeloid Differentiation Factor 88; D011971:Receptors, Immunologic / Q000276:immunology; D051197:Toll-Like Receptor 4 / Q000276:immunology; D051193:Toll-Like Receptors / Q000276:immunology*
D048868:Adaptor Proteins, Signal Transducing; D000943:Antigens, Differentiation; C507779:MYD88 protein, human; D053594:Myeloid Differentiation Factor 88; D011971:Receptors, Immunologic; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors