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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Regulatory T cells and minimal change nephropathy: in the midst of a complex network
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Regulatory T cells and minimal change nephropathy: in the midst of a complex network

机译：调节性T细胞和微小变化性肾病：处于复杂网络中

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摘要

Minimal change nephrosis (MCN) is an important cause of morbidity in children. In spite of successful therapies having been developed in the last three decades, most aspects related to pathogenesis still remain poorly defined. Evolution in basic immunology and results deriving from animal models of the disease suggest a complex interaction of factors and cells starting from activation of innate immunity and continuing with antigen presentation. Oxidants, CD80 and CD40/CD40L have probably a relevant role at the start. Studies in animal models and in human beings also suggest the possibility that the same molecules (i.e. CD80, CD40) are expressed by podocytes under inflammatory stimuli, representing a direct potential mechanism for proteinuria. B and T cells could play a relevant role this contest. Implication of B cells is suggested indirectly by studies utilizing anti-CD20 monoclonal antibodies as the main therapy. The role of regulatory T cells (T-regs) is supported mainly by results in animal models of nephrotic syndrome (i.e. adriamycin, puromycin, lipopolysaccharide), showing a protective effect of direct T-reg infusion or stimulation by interleukin 2 (IL-2). Limited studies have also shown reduced amounts of circulating T-regs in patients with active MCN cells. The route from bench to bedside would be reduced if results from animal models were confirmed in human pathology. The expansion of T-regs with recombinant IL-2 and new anti-CD20 monoclonal antibodies is the beginning. Blocking antigen-presenting cells with cytotoxic T lymphocyte antigen (CTLA-4)-Ig fusion molecules inhibiting CD80 and/or with blockers of CD40-CD40 ligand interaction represent potential new approaches. The hope is that evolution in therapies of MCN could fill a gap lasting 30 years.
机译：最小变化肾病（MCN）是儿童发病的重要原因。尽管在过去的三十年中已经开发出成功的疗法，但与发病机理有关的大多数方面仍不清楚。基本免疫学的演变和源自疾病动物模型的结果表明，从先天免疫的激活开始，一直到抗原呈递，因素与细胞之间的复杂相互作用。一开始，氧化剂CD80和CD40 / CD40L可能发挥了相关作用。在动物模型和人类中的研究还表明，在炎性刺激下足细胞表达相同分子（即CD80，CD40）的可能性，这是蛋白尿的直接潜在机制。 B和T细胞可能在这场比赛中发挥了重要作用。利用抗CD20单克隆抗体作为主要疗法的研究间接暗示了B细胞的涵义。调节性T细胞（T-regs）的作用主要由肾病综合征动物模型（即阿霉素，嘌呤霉素，脂多糖）的结果支持，显示直接T-reg输注或白介素2（IL-2）刺激的保护作用）。有限的研究还显示，活跃的MCN细胞患者体内循环T-reg的数量减少。如果在人类病理学中证实了动物模型的结果，将从长凳到床边的路线将减少。用重组IL-2和新的抗CD20单克隆抗体扩增T-regs是开始。用抑制CD80的细胞毒性T淋巴细胞抗原（CTLA-4）-Ig融合分子和/或用CD40-CD40配体相互作用的阻断剂阻断抗原呈递细胞代表了潜在的新方法。希望MCN疗法的发展可以填补持续30年的空白。

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