title: IL-13 production by allergen-stimulated T cells is increased in allergic disease and associated with IL-5 but not IFN-gamma expression.
abstract: Interleukin-13 (IL-13) shares many, but not all, of the properties of the prototypic T-helper type 2 (Th2) cytokine IL-4, but its role in allergen-driven T-cell responses remains poorly defined. We hypothesized that allergen stimulation of peripheral blood T cells from patients with atopic disease compared with non-atopic controls results in elevated IL-13 synthesis in the context of a 'Th2-type' pattern. Freshly isolated peripheral blood mononuclear cells (PBMC) obtained from sensitized atopic patients with allergic disease, and non-atopic control subjects, were cultured with the allergens Phleum pratense (Timothy grass pollen) or Dermatophagoides pteronyssinus (house dust mite) and the non-allergenic recall antigen Mycobacterium tuberculosis purified protein derivative (PPD). Supernatant concentrations of IL-13, along with IL-5 and interferon-gamma (IFN-gamma) (Th2- and Th1-type cytokines, respectively) were determined by enzyme-linked immunosorbent assay (ELISA). Allergen-induced IL-13 and IL-5 production by T cells from patients with allergic disease was markedly elevated (P = 0.0075 and P = 0.0004, respectively) compared with non-atopic controls, whereas IFN-gamma production was not significantly different. In contrast to allergen, the prototypic Th1-type antigen M. tuberculosis PPD induced an excess of IFN-gamma over IL-13 and IL-5 production, and absolute concentrations of cytokines were not affected by the presence or absence of atopic disease. Addition of exogenous recombinant IFN-gamma or IL-12, cytokines known to inhibit Th2-type responses, significantly inhibited allergen-driven production of both IL-13 and IL-5, but not T-cell proliferation, whereas exogenous IL-4 did not significantly affect production of IL-13 or IL-5. We conclude that allergen-specific T cells from atopic subjects secrete elevated quantities of IL-13 compared with non-atopic controls, in the context of a Th2-type pattern of cytokine production.
authors.affiliation: Imperial College School of Medicine, National Heart and Lung Institute, Houston, TX, USA.
authors.forename: S
authors.initials: S
authors.lastname: Till
authors.forename: S
authors.initials: S
authors.lastname: Durham
authors.forename: R
authors.initials: R
authors.lastname: Dickason
authors.forename: D
authors.initials: D
authors.lastname: Huston
authors.forename: J
authors.initials: J
authors.lastname: Bungre
authors.forename: S
authors.initials: S
authors.lastname: Walker
authors.forename: D
authors.initials: D
authors.lastname: Robinson
authors.forename: A B
authors.initials: AB
authors.lastname: Kay
authors.forename: C
authors.initials: C
authors.lastname: Corrigan
mesh_terms: D000485:Allergens / Q000276:immunology*; D018929:Cell Culture Techniques; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis*; D018793:Interleukin-13 / Q000096:biosynthesis*; D015848:Interleukin-5 / Q000096:biosynthesis*; D011058:Pollen / Q000276:immunology; D006255:Rhinitis, Allergic, Seasonal / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D014373:Tuberculin / Q000276:immunology
chemical_list: D000485:Allergens; D018793:Interleukin-13; D015848:Interleukin-5; D014373:Tuberculin; D007371:Interferon-gamma