Till S, Durham S, Dickason R, Huston D, Bungre J, Walker S, Robinson D, Kay A B, Corrigan C
Imperial College School of Medicine, National Heart and Lung Institute, Houston, TX, USA.
Immunology. 1997 May;91(1):53-7. doi: 10.1046/j.1365-2567.1997.00218.x.
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.
白细胞介素-13（IL-13）具有许多（但并非全部）典型的2型辅助性T细胞（Th2）细胞因子IL-4的特性，但其在变应原驱动的T细胞反应中的作用仍不清楚。我们推测，与非特应性对照相比，变应性疾病患者外周血T细胞受到变应原刺激后，会在“Th2型”模式下导致IL-13合成增加。从患有过敏性疾病的致敏变应性患者和非特应性对照受试者中获取新鲜分离的外周血单个核细胞（PBMC），将其与变应原梯牧草（梯牧草花粉）或粉尘螨（屋尘螨）以及非变应原性回忆抗原结核分枝杆菌纯化蛋白衍生物（PPD）一起培养。通过酶联免疫吸附测定（ELISA）测定IL-13以及IL-5和干扰素-γ（IFN-γ）（分别为Th2型和Th1型细胞因子）的上清液浓度。与非特应性对照相比，变应原诱导的变应性疾病患者T细胞产生的IL-13和IL-5明显升高（分别为P = 0.0075和P = 0.0004），而IFN-γ的产生没有显著差异。与变应原相反，典型的Th1型抗原结核分枝杆菌PPD诱导产生的IFN-γ超过IL-13和IL-5的产生，并且细胞因子的绝对浓度不受变应性疾病存在与否的影响。添加已知可抑制Th2型反应的外源性重组IFN-γ或IL-12，可显著抑制变应原驱动的IL-13和IL-5的产生，但不影响T细胞增殖，而外源性IL-4对IL-13或IL-5的产生没有显著影响。我们得出结论，在细胞因子产生的Th2型模式下，与非特应性对照相比，变应性受试者的变应原特异性T细胞分泌的IL-13量增加。
