Inhibition of autoimmune type 1 diabetes by gastrointestinal helminth infection
Inhibition of autoimmune type 1 diabetes by gastrointestinal helminth infection
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DOI：
10.1128/iai.00664-06
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发表时间：
2007-01-01
影响因子：
3.1
通讯作者：
Lawrence, Catherine E.
中科院分区：
文献类型：
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作者：
Saunders, Karin A.;Raine, Tim;Lawrence, Catherine E.
胃肠道线虫感染在世界范围内普遍存在，是T辅助2反应的有效诱导者，具有调节对异源抗原的免疫反应的能力。寄生蠕虫感染甚至被证明可以调节与自身免疫性疾病相关的免疫反应。非肥胖糖尿病(NOD)小鼠为研究人类自身免疫性糖尿病提供了一个模型；与人类一样，NOD小鼠糖尿病的发展与丧失对β细胞自身抗原的自身耐受性有关。之前对NOD小鼠的研究表明，地鼠和细菌感染似乎通过扰乱导致Th1介导的胰岛素产生的β细胞破坏的通路来抑制1型糖尿病。本研究的目的是观察感染旋毛虫和多回旋毛虫是否能抑制NOD小鼠自身免疫性糖尿病的发生，并分析其保护机制和Th2应答的作用。对糖尿病的保护是由蠕虫感染提供的，似乎通过扰乱导致β细胞破坏的途径来抑制自身免疫性糖尿病，并由看似独立的机制介导，具体取决于寄生虫，但这可能与宿主启动Th2反应的能力有关。
Gastrointestinal nematode infections are prevalent worldwide and are potent inducers of T helper 2 responses with the capacity to modulate the immune response to heterologous antigens. Parasitic helminth infection has even been shown to modulate the immune response associated with autoimmune diseases. Nonobese diabetic (NOD) mice provide a model for studying human autoimmune diabetes; as in humans, the development of diabetes in NOD mice has been linked to the loss of self-tolerance to beta cell autoantigens. Previous studies with the NOD mouse have shown that belminth and bacterial infection appears to inhibit type 1 diabetes by disrupting the pathways leading to the Th1-mediated destruction of insulin-producing beta cells. The aim of our study was to examine whether infection with the gastrointestinal helminths Trichinella spiralis or Heligmosomoides polygyrus could inhibit the development of autoimmune diabetes in NOD mice and to analyze the mechanisms involved in protection and the role of Th2 responses. Protection from diabetes was afforded by helminth infection, appeared to inhibit autoimmune diabetes by disrupting pathways leading to the destruction of beta cells, and was mediated by seemingly independent mechanisms depending on the parasite but which may be to be related to the capacity of the host to mount a Th2 response.