title: Toll-like receptors and T-helper-1/T-helper-2 responses.
abstract: OBJECTIVE
  Toll-like receptors (TLRs) are a family of pattern recognition receptors that are activated by specific components of microbes and certain host molecules. They constitute the first line of defense against many pathogens and play a crucial role in the function of the innate immune system. Recently, TLRs were observed to influence the development of adaptive immune responses, presumably by activating antigen-presenting cells. This has important implications for our understanding of how the host tailors its immune response as a function of specific pathogen recognition. The present review discusses the recent studies that demonstrate the role of TLRs in the regulation of adaptive T-helper-1 (Th1) and Th2 responses, and the mechanisms by which the effects are carried out.
  
  
  RESULTS
  Most studies have focused on the role of TLRs and components of their signaling pathways in the control of Th1-type immune responses, and on the implications for their use as antimicrobial agents, such as adjuvants in vaccines, or to treat or prevent the Th2-type dominated immune responses seen in allergies. TLR-deficient mice have been described and used to come to these conclusions. Although controversial, there is also evidence that TLRs may be important for Th2-type responses, possibly by augmenting the overall maturity of dendritic cells.
  
  
  CONCLUSIONS
  A greater understanding of the processes by which TLRs regulate adaptive immunity may yield not only improved ways to treat infectious diseases but also new approaches to the treatment and prevention of allergic and certain autoimmune disorders.
authors.affiliation: Respiratory Diseases, Roche Palo Alto, Palo Alto, California 94304, USA. karim.dabbagh@roche.com
authors.forename: Karim
authors.initials: K
authors.lastname: Dabbagh
authors.forename: David B
authors.initials: DB
authors.lastname: Lewis
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology / Q000378:metabolism; D001419:Bacteria / Q000737:chemistry / Q000276:immunology; D007113:Immunity, Innate; D007378:Interleukins / Q000145:classification / Q000276:immunology / Q000378:metabolism; D008213:Lymphocyte Activation / Q000276:immunology; D008562:Membrane Glycoproteins / Q000145:classification / Q000276:immunology / Q000502:physiology*; D051379:Mice; D011956:Receptors, Cell Surface / Q000145:classification / Q000276:immunology / Q000502:physiology*; D015398:Signal Transduction / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology* / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology* / Q000378:metabolism; D051193:Toll-Like Receptors
chemical_list: D007378:Interleukins; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors