Lymphokine production by human T cells in disease states.
A large body of evidence suggests the existence of polarized human T cell responses, reminiscent of Th1 and Th2 subsets described for mouse T cells. Human Th1-like cells preferentially develop during infections by intracellular bacteria, protozoa, and viruses, whereas Th2-like cells predominate during helminthic infestations and in response to common environmental allergens. The cytokine profile of "natural immunity" evoked by different offending agents in the context of different host genetic backgrounds appears to be a critical factor in determining the phenotype of the subsequent specific response. Strongly polarized human Th1-type and Th2-type responses not only play different roles in protection, they can also promote different immunopathological reactions. Th1-type responses appear to be involved in organ specific autoimmunity, in contact dermatitis, and in some chronic inflammatory disorders of unknown etiology. In contrast, in genetically predisposed hosts, Th2-type responses against common environmental allergens are responsible for triggering of allergic atopic disorders. Altered profiles of lymphokine production may account for immune dysfunctions in some primary or acquired immunodeficiency syndromes. The role of lymphokines produced by T cells in the pathogenesis of systemic autoimmune disorders is less clear. Further work is also required to better clarify the role of T cell-derived lymphokines in protecting against tumors or in favoring their development.
Division of Clinical Immunology and Allergy, University of Florence, Italy.
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Romagnani
D001327:Autoimmune Diseases / Q000276:immunology; D006084:Graft Rejection / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology; D007154:Immune System Diseases / Q000276:immunology*; D007153:Immunologic Deficiency Syndromes / Q000276:immunology; D007239:Infections / Q000276:immunology*; D007249:Inflammation / Q000276:immunology; D008222:Lymphokines / Q000502:physiology*; D009369:Neoplasms / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000502:physiology*
D008222:Lymphokines