根據(jù)來自美國新澤西口腔醫(yī)科大學(xué)新澤西醫(yī)學(xué)院(University of Medicine and Dentistry of New Jersey-New Jersey Medical School)的William Gause博士和同事們完成的一項(xiàng)研究,，短期的腸道蠕蟲感染可能給予身體長期抵抗I型糖尿病(type I diabetes, TID)的保護(hù),。這項(xiàng)研究于2012年7月18日在線發(fā)表在Mucosal Immunology期刊上。
TID是由于身體自己的免疫細(xì)胞攻擊產(chǎn)胰島素的胰島細(xì)胞而產(chǎn)生的。在發(fā)展中國家,，TID發(fā)生率相對(duì)較低。對(duì)這種現(xiàn)象的一種解釋就是普遍存在慢性腸道蠕蟲感染,，而這種感染破壞導(dǎo)致導(dǎo)致糖尿病和其他自身免疫疾病產(chǎn)生的自我攻擊性T細(xì)胞,。理解在蠕蟲感染期間T細(xì)胞如何遭到破壞將可能導(dǎo)致人們開發(fā)出新的策略來控制這些炎癥性疾病。
Gause博士領(lǐng)導(dǎo)的一個(gè)研究小組證實(shí)遭受腸道蠕蟲---即多形螺旋線蟲(H. polygyru),，可利用口服藥物進(jìn)行治療---兩周感染促進(jìn)T細(xì)胞產(chǎn)生細(xì)胞因子白細(xì)胞介素4(interleukin-4, IL-4)和IL-10,，這兩種細(xì)胞因子獨(dú)立發(fā)揮作用而給小鼠給予持久性地抵抗TID的保護(hù)。如今,，這項(xiàng)研究提供一種潛在的機(jī)制來解釋利用寄生性蠕蟲感染來控制炎癥性疾病的能力,。(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.
