Inada S, Yoshino S, Haque M A, Ogata Y, Kohashi O
Department of Microbiology, Saga Medical School, Japan.
Cell Immunol. 1997 Jan 10;175(1):67-75. doi: 10.1006/cimm.1996.1049.
The effects of oral administration of ovalbumin (OVA) on acute OVA-induced arthritis (OIA) in rats, which is mediated by Arthus reaction to the antigen in the joint space, were investigated. The oral administration of OVA before immunization with OVA significantly suppressed the development of acute OIA in a dose-dependent manner, in accordance with decreases in both the in vivo anti-OVA IgG antibody production and in vitro lymphocyte proliferative responses to OVA. These results were shown in both the single high-dose (200 mg x 1) or the multiple low-dose (200 microg x 5) feeding protocols. In vitro study showed that rat IL-2 could reverse the reduced OVA-specific lymphocyte proliferative responses. The spleen cells obtained from OVA-feeding, unprimed rats neither adoptively transferred the suppression to naive recipient rats nor suppressed the in vitro lymphocyte proliferation. These results demonstrate that the acute OIA can be suppressed by the induction of oral tolerance (OT) to OVA, and strongly suggest that the OT was due to clonal anergy of antigen-reactive T lymphocytes, not the active suppression by OVA-specific regulatory cells.
研究了口服卵清蛋白（OVA）对大鼠急性OVA诱导性关节炎（OIA）的影响，该关节炎由关节腔内对抗原的Arthus反应介导。在OVA免疫前口服OVA，根据体内抗OVA IgG抗体产生和体外淋巴细胞对OVA增殖反应的降低，以剂量依赖方式显著抑制急性OIA的发展。在单次高剂量（200mg×1）或多次低剂量（200μg×5）喂养方案中均显示出这些结果。体外研究表明，大鼠IL-2可逆转降低的OVA特异性淋巴细胞增殖反应。从喂食OVA、未致敏的大鼠获得的脾细胞既未将抑制作用过继转移至未致敏的受体大鼠，也未抑制体外淋巴细胞增殖。这些结果表明，急性OIA可通过诱导对OVA的口服耐受（OT）来抑制，并强烈提示OT是由于抗原反应性T淋巴细胞的克隆无能，而非OVA特异性调节细胞的主动抑制。
