title: Do microbes influence the pathogenesis of allergic diseases? Building the case for Toll-like receptor ligands.
abstract: The prevalence and severity of allergic diseases and other diseases of immune dysregulation are increasing in industrialized countries. One explanation for these trends is that decreased exposure to microbes, due to modern public health practices, has resulted in the loss of a main source of immune provocation, and a consequent increase in pathogenic immune responses and their associated diseases. It is now clear that molecular interactions between immunocytes and microbes are mediated largely by Toll-like receptors (TLRs) on host cells and a diversity of ligands produced by viruses, bacteria and fungi. Physiological exposures to TLR ligands are also likely to have an important yet complex role in host immune homeostasis and predisposition towards atopy.
authors: University of California, San Diego, 9500 Gilman Drive, Mail code 0663, La Jolla, CA 92093-0663, USA. ahorner@ucsd.edu
authors: Anthony A
authors: AA
authors: Horner
authors: Eyal
authors: E
authors: Raz
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000943:Antigens, Differentiation / Q000378:metabolism; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology / Q000378:metabolism / Q000382:microbiology*; D008024:Ligands; D008070:Lipopolysaccharides / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism*; D053594:Myeloid Differentiation Factor 88; D011956:Receptors, Cell Surface / Q000378:metabolism*; D011971:Receptors, Immunologic / Q000378:metabolism; D051193:Toll-Like Receptors
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D000943:Antigens, Differentiation; D008024:Ligands; D008070:Lipopolysaccharides; C507779:MYD88 protein, human; D008562:Membrane Glycoproteins; D053594:Myeloid Differentiation Factor 88; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; D051193:Toll-Like Receptors