首页> 美国卫生研究院文献>Clinical and Experimental Immunology >A transient rise in agalactosyl IgG correlating with free interleukin 2 receptors during episodes of erythema nodosum leprosum.
【2h】

A transient rise in agalactosyl IgG correlating with free interleukin 2 receptors during episodes of erythema nodosum leprosum.

机译:在结节性红斑性麻风发作期间半乳糖基IgG的短暂升高与游离的白介素2受体相关。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

The proportion of oligosaccharide chains on the Fc fragment of IgG which terminate with N-acetylglucosamine and not galactose (%GO) has previously been shown to be raised in rheumatoid arthritis (RA), Crohn's disease (CD) and tuberculosis (Tb), but to be normal in sarcoidosis (SA), and in both lepromatous and tuberculoid leprosy. However we have now studied %GO in sequential serum samples collected from lepromatous leprosy patients undergoing episodes of erythema nodosum leprosum (ENL). During ENL %GO is transiently raised, and this rise parallels an increase in circulating interleukin 2 receptors (IL-2R). These findings confirm that changes in T cell function occur during ENL. Moreover it appears that %GO rises when there is, simultaneously, T-cell-mediated tissue damage and an acute phase response (RA, CD, Tb, ENL), but not when there is an acute phase response without major T cell involvement, or chronic T cell activity alone (SA, and tuberculoid leprosy). We suggest therefore that %GO is an indicator of a type of T cell activity with broad immunopathological implications.
机译:IgG的Fc片段上以N-乙酰氨基葡糖而非半乳糖(%GO)终止的寡糖链的比例先前已证明在类风湿性关节炎(RA),克罗恩氏病(CD)和肺结核(Tb)中升高,但是在结节病(SA),麻风病和结核性麻风病中均正常。但是,我们现在已经从经历了红斑结节性麻风病(ENL)发作的麻风病麻风病患者的连续血清样本中研究了%GO。在ENL期间,%GO短暂升高,并且该升高与循环白介素2受体(IL-2R)的升高平行。这些发现证实在ENL期间T细胞功能发生了改变。此外,当同时存在T细胞介导的组织损伤和急性期反应(RA,CD,Tb,ENL)时,%GO升高,而在没有主要T细胞参与的急性期反应中却没有升高,或单独的慢性T细胞活动(SA和结核性麻风)。因此,我们建议%GO是具有广泛免疫病理意义的T细胞活性类型的指标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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