梭菌属细菌促发小鼠结肠调节性T细胞有望治疗某些自身免疫性疾病
2010-12-27 20:03:00 来源：丁香园 作者： 评论：0 点击：
无数个把我们的身体称作“家”的微生物究竟怎样帮助我们维持健康的免疫系统? 一项在小鼠身上所做的新的研究显示，梭菌属的特别细菌会促进小鼠结肠中的调节性T细胞(或Treg细胞)的产生，这一发现提示了对过敏和自身免疫反应的新的治疗方法。 Koji Atarashi及其同事首先清除了小鼠结肠中的所有细菌。他们发现小鼠结肠的Treg细胞数目发生了骤降。 通过给这些无菌小鼠定量施予某一梭菌属菌株的混合物，研究人员观察到那些Treg细胞回归到了结肠。 研究人员还发现，给野生型小鼠(即它们所有的共生菌都是完好的)喂养梭菌属细菌会在小鼠中增高其Treg细胞的水平，并帮助小鼠避免发生自身免疫性大肠炎和其它过敏症。 这些数据凸显了这些特别的梭菌属细菌是如何帮助调节特别的免疫细胞组群的。将来，这些发现甚至可被用来改善对某些自身免疫性疾病的治疗。
梭菌属细菌
文字说明: 小鼠结肠的梭菌属细菌种刺激肠上皮细胞分泌 TGF-b，造成Foxp3表达的T细胞的累积以及IL -10在结肠的产生，这有助于抑制炎症和过敏性反应。
资料来源: 《科学》/美国科学促进会
使用限制: 请注明图片所有者。这张图片可以供记者适当的自由使用在新闻报导，非记者人员请联系《科学》以获得图片使用权
One bacterium brings on the T cells
How exactly do the countless microbes that call our bodies "home" help us to maintain healthy immune systems? A new study with mice has shown that specific bacteria of the genus Clostridium promote the generation of regulatory T cells, or Treg cells, in the mouse colon—a discovery that suggests new therapeutic approaches to allergies and autoimmunity. Koji Atarashi and colleagues first eliminated all the bacteria from the colons of mice and found that populations of colonic Treg cells plummeted. By dosing those bacteria-free mice with a certain mix of Clostridium strains, the researchers observed a return of those Treg cells to the colon. The researchers also found that feeding wild-type mice (with all their commensal bacteria intact) the Clostridium bacteria produced elevated levels of Treg cells in the mice and helped the rodents to ward off autoimmune colitis and other allergies. These data highlight how these particular Clostridium bacteria help to regulate specific immune cell populations, and in the future the findings might even be used to improve treatment for certain autoimmune diseases.
###
Article #22: "Induction of colonic regulatory T cells by indigenous Clostridium species," by K. Atarashi; T. Tanoue; T. Taniguchi; K. Honda; Y. Momose; K. Itoh at The University of Tokyo in Tokyo, Japan; T. Shima; A. Imaoka; Y. Umesaki at Yakult Central Institute for Microbiological Research in Tokyo, Japan; T. Kuwahara at The University of Tokushima Graduate School in Tokushima, Japan; K. Takeda at University of California, Los Angeles in Los Angeles, CA; S. Yamasaki; T. Saito; S. Hori at RIKEN Research Center for Allergy and Immunology in Yokohama, Japan; Y. Ohba at Graduate School of Medicine, Hokkaido University in Sapporo, Japan; I.I. Ivanov at Columbia University Medical Center in New York, NY; K. Honda at Japan Science and Technology Agency in Saitama, Japan.
文字说明: 小鼠结肠的梭菌属细菌种刺激肠上皮细胞分泌 TGF-b，造成Foxp3表达的T细胞的累积以及IL -10在结肠的产生，这有助于抑制炎症和过敏性反应。
资料来源: 《科学》/美国科学促进会
使用限制: 请注明图片所有者。这张图片可以供记者适当的自由使用在新闻报导，非记者人员请联系《科学》以获得图片使用权
One bacterium brings on the T cells
How exactly do the countless microbes that call our bodies "home" help us to maintain healthy immune systems? A new study with mice has shown that specific bacteria of the genus Clostridium promote the generation of regulatory T cells, or Treg cells, in the mouse colon—a discovery that suggests new therapeutic approaches to allergies and autoimmunity. Koji Atarashi and colleagues first eliminated all the bacteria from the colons of mice and found that populations of colonic Treg cells plummeted. By dosing those bacteria-free mice with a certain mix of Clostridium strains, the researchers observed a return of those Treg cells to the colon. The researchers also found that feeding wild-type mice (with all their commensal bacteria intact) the Clostridium bacteria produced elevated levels of Treg cells in the mice and helped the rodents to ward off autoimmune colitis and other allergies. These data highlight how these particular Clostridium bacteria help to regulate specific immune cell populations, and in the future the findings might even be used to improve treatment for certain autoimmune diseases.
###
Article #22: "Induction of colonic regulatory T cells by indigenous Clostridium species," by K. Atarashi; T. Tanoue; T. Taniguchi; K. Honda; Y. Momose; K. Itoh at The University of Tokyo in Tokyo, Japan; T. Shima; A. Imaoka; Y. Umesaki at Yakult Central Institute for Microbiological Research in Tokyo, Japan; T. Kuwahara at The University of Tokushima Graduate School in Tokushima, Japan; K. Takeda at University of California, Los Angeles in Los Angeles, CA; S. Yamasaki; T. Saito; S. Hori at RIKEN Research Center for Allergy and Immunology in Yokohama, Japan; Y. Ohba at Graduate School of Medicine, Hokkaido University in Sapporo, Japan; I.I. Ivanov at Columbia University Medical Center in New York, NY; K. Honda at Japan Science and Technology Agency in Saitama, Japan.
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