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Peripheral deletion of antigen-reactive T cells in oral tolerance.

机译：口服耐受性中抗原反应性T细胞的周边缺失。

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摘要

Oral administration of antigen is used to induce antigen-specific peripheral immune tolerance. As well as preventing systemic immune responses to ingested proteins, oral tolerance to autoantigens has also been used to suppress autoimmune diseases in animals and humans. Both active suppression and clonal anergy are suggested to be mechanisms of oral tolerance, depending on the dose of antigen fed. Here we report that oral antigen can delete antigen-reactive T cells in Peyer's patches, in mice transgenic for the ovalbumin-specific T-cell receptor genes. The deletion was mediated by apoptosis, and was dependent on dosage and frequency of feeding. At lower doses deletion was not observed; instead there was induction of antigen-specific cells that produced transforming growth factor (TGF)-beta and interleukin (IL)-4 and IL-10 cytokines. At higher doses, both Th1 and Th2 cells were deleted following their initial activation, whereas cells which secrete TGF-beta were resistant to deletion. These findings demonstrate that orally administered antigen can induce tolerance not only by active suppression and clonal anergy but by extrathymic deletion of antigen-reactive Th1 and Th2 cells.
机译：口服抗原用于诱导抗原特异性外周免疫耐受。除了防止对摄入蛋白质的全身免疫反应外，对自身抗原的口服耐受性也已被用于抑制动物和人类的自身免疫性疾病。主动抑制和克隆性无能都被认为是口服耐受的机制，这取决于抗原的剂量。在这里我们报告说，口服卵清蛋白可以在卵白蛋白特异性T细胞受体基因转基因的小鼠中删除Peyer斑中的抗原反应性T细胞。缺失是由细胞凋亡介导的，并且取决于剂量和喂养频率。在较低剂量下未观察到缺失。取而代之的是诱导抗原特异性细胞，这些细胞产生转化生长因子（TGF）-β和白介素（IL）-4和IL-10细胞因子。在较高剂量下，Th1和Th2细胞在初始激活后均被删除，而分泌TGF-β的细胞对删除具有抗性。这些发现表明，口服给予的抗原不仅可以通过主动抑制和克隆无能，而且可以通过胸腺外删除抗原反应性Th1和Th2细胞来诱导耐受。

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