Intestinal nematode parasites, cytokines and effector mechanisms.
Laboratory models of intestinal nematode infection have played an important role in developing our understanding of the immune mechanisms that operate against infectious agents. The type of helper T cell response that develops following infection with intestinal nematode parasites is critical to the outcome of infection. The early events that mediate polarisation of the helper T cell subsets towards either Th1 or Th2 during intestinal nematode infection are not well characterised, but it is likely that multiple factors influence the induction of a Th1 or Th2 type response, just as multiple effector mechanisms are involved in worm expulsion. Costimulatory molecules have been shown to be important in driving T helper cell development down a specific pathway as has the immediate cytokine environment during T cell activation. If helper T cells of the Th2 type gain ascendancy then a protective immune response ensues, mediated by Th2 type cytokines and the effector mechanisms they control. In contrast, if an inappropriate Th1 type response predominates the ability to expel infection is compromised. Equally important is the observation that multiple potential effector mechanisms are stimulated by nematode infection, with a unique combination operating against the parasite depending on nematode species and its life cycle stage. Despite the close association between intestinal nematode infection and the generation of eosinophilia, mastocytosis and IgE it has been difficult to consistently demonstrate a role for these effector cells/molecules in resistance to nematode parasites, although mast cells are clearly important in some cases. It therefore seems that, in general, less classical Th2 controlled effector mechanisms, which remain poorly defined, are probably important in resistance to nematode parasites. Thus, our understanding of both the induction and effector phases remains incomplete and will remain an intense area of interest in the coming years.
Else
K J
KJ
School of Biological Sciences, University of Manchester, U.K. Kathryn.J.Else@man.ac.uk
Finkelman
F D
FD
D000818:Animals; D000909:Antibodies, Helminth / Q000097:blood / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology; D016207:Cytokines / Q000276:immunology*; D004804:Eosinophils / Q000502:physiology; D020397:Goblet Cells / Q000378:metabolism; D006790:Host-Parasite Interactions; D007411:Intestinal Diseases, Parasitic / Q000276:immunology*; D008407:Mast Cells / Q000502:physiology; D051379:Mice; D009077:Mucins / Q000378:metabolism / Q000502:physiology; D009348:Nematoda / Q000276:immunology* / Q000502:physiology; D009349:Nematode Infections / Q000276:immunology*; D051381:Rats; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology*
D000909:Antibodies, Helminth; D016207:Cytokines; D009077:Mucins