CD4+ T-cell dynamics and host predisposition to infection.
Resistance to infection is often associated with proliferative T-cell responses corresponding to activation of the Th1 CD4+ T-cell subset, while the proliferative responses of chronically infected individuals are often limited. A mathematical model of the interaction between Th1 cells and a replicating pathogen has been used to demonstrate that antigen dose-dependent inhibition of Th1-cell proliferation may differentially predispose the host to resistance or chronic infection according to the level of exposure. Furthermore, the rapidity of pathogen turnover dramatically influences the qualitative relationship between exposure level and outcome, the temporal progression of infection, and the extent to which superimposed regulation of effector function (distinct from proliferation) will alter the predicted predisposition.
Schweitzer
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Department of Biology, Imperial College, London, United Kingdom.
D000953:Antigens, Protozoan / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D016207:Cytokines / Q000502:physiology; D004306:Dose-Response Relationship, Immunologic; D007113:Immunity, Innate; D007239:Infections / Q000276:immunology*; D007371:Interferon-gamma / Q000096:biosynthesis*; D007896:Leishmaniasis / Q000276:immunology; D008213:Lymphocyte Activation; D008962:Models, Theoretical; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology*; D013997:Time Factors
D000953:Antigens, Protozoan; D016207:Cytokines; D007371:Interferon-gamma