Van Houten N, Blake S F
Department of Internal Medicine, Galveston 77555-0366, USA.
J Immunol. 1996 Aug 15;157(4):1337-41.
T cell tolerance induced by oral administration of Ag may be the result of either deletion or functional inactivation of Ag-specific T cells. OVA p(323-339)-specific TCR transgenic (Tg+) lymphocytes were transplanted into BALB/c recipients. Chimeric mice were fed OVA and subsequently challenged with the peptide in CFA. Tolerance was then assessed by measurement of lymph node (LN) cell proliferation in response to the peptide, and deletion was assessed by measuring the frequency Tg+ T cells by flow cytometry. Lymphocytes from chimeric mice fed OVA showed a dose-dependent decline in their proliferative response to the peptide in vitro, compared with immunized control mice that were not fed OVA. Calculation of proliferative potential per Tg+ cell demonstrates that nonresponsiveness due to feeding Ag results in the induction of anergy in the LN. In addition, analysis of intestinal intraepithelial lymphocytes following feeding of OVA did not show evidence of trafficking of LN T cells to the small intestine intraepithelial nor lamina propria compartments.
口服抗原诱导的T细胞耐受性可能是抗原特异性T细胞缺失或功能失活的结果。将卵清蛋白（OVA）p(323 - 339)特异性T细胞受体转基因（Tg+）淋巴细胞移植到BALB/c受体小鼠体内。给嵌合小鼠喂食OVA，随后用该肽与弗氏完全佐剂（CFA）进行攻击。然后通过测量淋巴结（LN）细胞对该肽的增殖反应来评估耐受性，并通过流式细胞术测量Tg+ T细胞的频率来评估缺失情况。与未喂食OVA的免疫对照小鼠相比，喂食OVA的嵌合小鼠的淋巴细胞在体外对该肽的增殖反应呈剂量依赖性下降。计算每个Tg+细胞的增殖潜能表明，由于喂食抗原导致的无反应性会在LN中诱导无能。此外,在喂食OVA后对肠道上皮内淋巴细胞的分析未显示LN T细胞向小肠上皮内或固有层区室迁移的证据。
