...
首页> 外文期刊>The Journal of Experomental Medicine >Differential major histocompatibility complex-related activation of idiotypic suppressor T cells. Suppressor T cells cross-reactive to two distantly related lysozymes are not induced by one of them.
【24h】

Differential major histocompatibility complex-related activation of idiotypic suppressor T cells. Suppressor T cells cross-reactive to two distantly related lysozymes are not induced by one of them.

机译:差异性主要组织相容性复合物相关的独特型抑制性T细胞活化。抑制性T细胞对两种远距离相关的溶菌酶均具有交叉反应性,而其中之一则不会诱导这种抑制性T细胞。

获取原文
   

获取外文期刊封面封底 >>

       

摘要

B10 (H-2b) mice are genetic nonresponders to hen egg-white lysozyme (HEL) and the distantly related human lysozyme (HUL). However, anti-HEL or anti-HUL primary antibody responses in vivo or in vitro can be obtained in B10 mice by immunization with the appropriate lysozyme coupled to erythrocytes. T cells able to suppress either anti-lysozyme plaque-forming cells (PFC) response are induced in B10 mice after immunization with HEL-complete Freund's adjuvant (CFA) or HUL-CFA. This cross-reactivity of HEL and HUL in the induction and the expression of suppressive activity is in marked contrast to their very low cross-reactivity at the PFC level. These results suggest that either HEL or HUL can stimulate a suppressor T cell which recognizes a particular epitope present on both lysozymes. Suppressor cells induced by HEL or HUL bear the same predominant idiotype found on the majority of anti-HEL antibodies, and on the small proportion of anti-HUL antibodies cross-reactive with HEL. B10.Q (H-2q) mice are responders in vivo to HEL-CFA, but not to HUL-CFA. In contrast to B10, HEL-CFA priming in B10.Q micr induces helper cells whereas HUL-CFA priming induces suppressor cells. These suppressor cells are cross-reactive with HEL and are fully able to suppress HEL-specific helper cells. The presence of HEL-specific suppressor cell precursors in B10.Q mice which are not activated by HEL, seems to implicate differential choice by the antigen presenting system as a basis for Ir gene control, rather than the absence of a regulatory cell type from the T cell repertoire.
机译:B10(H-2b)小鼠是对鸡蛋清溶菌酶(HEL)和远缘相关的人溶菌酶(HUL)的遗传无反应者。但是,通过用偶联至红细胞的适当溶菌酶进行免疫,可以在B10小鼠中获得体内或体外的抗HEL或抗HUL一级抗体应答。在用HEL-完全弗氏佐剂(CFA)或HUL-CFA免疫后,在B10小鼠中诱导了能够抑制抗溶菌酶斑块形成细胞(PFC)反应的T细胞。 HEL和HUL在诱导中的这种交叉反应性和抑制活性的表达与它们在PFC水平上非常低的交叉反应性形成鲜明对比。这些结果表明,HEL或HUL均可刺激抑制性T细胞,后者识别两种溶菌酶上均存在的特定表位。由HEL或HUL诱导的抑制细胞具有与大多数抗HEL抗体相同的优势独特型,以及与HEL发生交叉反应的小比例的抗HUL抗体。 B10.Q(H-2q)小鼠在体内对HEL-CFA有反应,但对HUL-CFA不是。与B10相反,B10.Q micr中的HEL-CFA启动引发了辅助细胞,而HUL-CFA启动引发了抑制性细胞。这些抑制细胞可与HEL发生交叉反应,并完全能够抑制HEL特异性辅助细胞。没有被HEL激活的B10.Q小鼠中HEL特异性抑制细胞前体的存在似乎暗示了抗原呈递系统的差异选择是Ir基因控制的基础,而不是因为没有特定的调节细胞类型。 T细胞库。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号