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葡萄球菌肠毒素B可诱导雌性DBA/1小鼠患关节炎,但不能诱导II型胶原反应性淋巴细胞的激活。

Staphylococcal enterotoxin B induces arthritis in female DBA/1 mice but fails to induce activation of type II collagen-reactive lymphocytes.

作者信息

Omata S, Sasaki T, Kakimoto K, Yamashita U

机构信息

Department of Immunology, University of Occupational and Environmental Health, School of Medicine, Kitakyusyu, Japan.

出版信息

Cell Immunol. 1997 Aug 1;179(2):138-45. doi: 10.1006/cimm.1997.1164.

Abstract

It has been proposed that superantigens are involved in the pathogenesis of autoimmune diseases. To test the possibility of superantigens inducing arthritis in naive mice, V beta 8-reactive superantigen staphylococcal enterotoxin B (SEB) was injected into naive mice. We used female DBA/1 mice, because they were susceptible to collagen-induced arthritis (CIA), in which the pathogenic T cells were supposed to preferentially use limited V betas of T cell receptors including V beta 8. Mild monoarthritis developed in uninjected hindlimbs of mice administered with SEB in higher frequency (an average incidence of 24%) than the control phosphate-buffered saline-injected mice (4.2%). Autoimmune responses in mice administered with SEB were compared with those in mice developing CIA. However, activation of type II collagen (IIC)-reactive T cells was not detected in SEB-injected mice. Production of autoantibodies, anti-IIC antibody and rheumatoid factor was also undetected. Although exact mechanisms of pathogenesis of this arthritis remain to be known, V beta 8+ T cells were activated for a long period and the unresponsiveness of V beta 8+ T cells was not detected in this strain. From these results, we discuss the pathogenesis of arthritis induced by SEB and the possibility that superantigen may play a role in the induction of autoimmune diseases.

摘要

有人提出超抗原参与自身免疫性疾病的发病机制。为了测试超抗原在未接触过抗原的小鼠中诱发关节炎的可能性,将Vβ8反应性超抗原葡萄球菌肠毒素B(SEB)注射到未接触过抗原的小鼠体内。我们使用雌性DBA/1小鼠,因为它们易患胶原诱导的关节炎(CIA),在这种关节炎中,致病性T细胞被认为优先使用包括Vβ8在内的有限数量的T细胞受体Vβ。与注射对照磷酸盐缓冲盐水的小鼠(4.2%)相比,接受SEB注射的小鼠未注射的后肢更频繁地出现轻度单关节炎(平均发病率为24%)。将接受SEB注射的小鼠的自身免疫反应与患CIA的小鼠的自身免疫反应进行了比较。然而,在注射SEB的小鼠中未检测到II型胶原(IIC)反应性T细胞的激活。也未检测到自身抗体、抗IIC抗体和类风湿因子的产生。尽管这种关节炎的确切发病机制尚不清楚,但Vβ8 + T细胞被长期激活,并且在该品系中未检测到Vβ8 + T细胞的无反应性。根据这些结果,我们讨论了SEB诱导的关节炎的发病机制以及超抗原可能在自身免疫性疾病诱导中发挥作用的可能性。

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