根据来自美国新泽西口腔医科大学新泽西医学院(University of Medicine and Dentistry of New Jersey-New Jersey Medical School)的William Gause博士和同事们完成的一项研究，短期的肠道蠕虫感染可能给予身体长期抵抗I型糖尿病(type I diabetes, TID)的保护。这项研究于2012年7月18日在线发表在Mucosal Immunology期刊上。
TID是由于身体自己的免疫细胞攻击产胰岛素的胰岛细胞而产生的。在发展中国家，TID发生率相对较低。对这种现象的一种解释就是普遍存在慢性肠道蠕虫感染，而这种感染破坏导致导致糖尿病和其他自身免疫疾病产生的自我攻击性T细胞。理解在蠕虫感染期间T细胞如何遭到破坏将可能导致人们开发出新的策略来控制这些炎症性疾病。
Gause博士领导的一个研究小组证实遭受肠道蠕虫---即多形螺旋线虫(H. polygyru)，可利用口服药物进行治疗---两周感染促进T细胞产生细胞因子白细胞介素4(interleukin-4, IL-4)和IL-10，这两种细胞因子独立发挥作用而给小鼠给予持久性地抵抗TID的保护。如今，这项研究提供一种潜在的机制来解释利用寄生性蠕虫感染来控制炎症性疾病的能力。(生物谷：Bioon.com)
doi:10.1038/mi.2012.71
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Prevention of type 1 diabetes through infection with an intestinal nematode parasite requires IL-10 in the absence of a Th2-type response
P K Mishra1, N Patel1, W Wu1, D Bleich2,3 and W C Gause
Helminth infection can prevent type 1 diabetes (T1D); however, the regulatory mechanisms inhibiting disease remain largely undefined. In these studies, nonobese diabetic (NOD) IL-4−/− mice were infected with the strictly enteric nematode parasite, Heligmosomoides polygyrus. Short-term infection, 5–7 weeks of age, inhibited T1D onset, as late as 40 weeks of age. CD4+ T-cell STAT6 phosphorylation was inhibited, while suppressed signal transducer and activator of transcription 1 phosphorylation was sustained, as were increases in FOXP3−, CD4+ T-cell interleukin (IL)-10 production. Blockade of IL-10 signaling in NOD-IL-4−/−, but not in NOD, mice during this short interval abrogated protective effects resulting in pancreatic β-cell destruction and ultimately T1D. Transfer of CD4+ T cells from H. polygyrus (Hp)-inoculated NOD IL-4−/− mice to NOD mice blocked the onset of T1D. These studies indicate that Hp infection induces non-T-regulatory cells to produce IL-10 independently of STAT6 signaling and that in this Th2-deficient environment IL-10 is essential for T1D inhibition.
