蠕虫及蠕虫源性分子可对多种自身免疫性疾病具有预防和改善作用，但其作用机制尚不清楚。炎症性肠病(IBD)是因患者肠黏膜免疫系统反应过度而导致组织损害。前期研究表明，旋毛虫排泄分泌抗原（TsES）及副肌球蛋白（TsPmy）能够诱导Treg的产生，并能够缓解葡聚糖硫酸钠（DSS）诱导的溃疡性结肠炎（UC）。由此，我们提出科学假设：“蠕虫疗法”可通过诱导肠道区域性Treg细胞的产生建立免疫稳态，从而抑制IBD的发生发展。本研究通过观察TsES和TsPmy诱导的肠道区域性Treg细胞在抑制UC过程中的作用，明确该群肠道区域性Treg细胞的功能，进而阐明该群Treg细胞之于UC的作用机制。本课题将为肠道区域免疫特性结合传统的黏膜免疫系统发挥免疫作用提供新的理论依据，同时将进一步完善 “蠕虫疗法”的分子机制，为开发虫源分子抗原作为免疫抑制药物发挥靶向治疗IBD以及其他免疫性疾病提供实验依据。

Helminth and helminth derived molecules could contribute to the precaution and improvement in the progression of autoimmune disease, however, the mechanism need to be further determined. Inflammatory bowel disease(IBD) is caused by that the intestinal mucosal immune system executes overreaction which results in tissue lesion. Our previous study indicated that excretory/secretory antigens of Trichinella spiralis (TsES) and paramyosin of Trichinella spiralis (TsPmy) could induce the production of Treg, and facilitate anesis in ulcerative colitis (UC) simulated by dextran sulphate sodium (DSS). Therefore, we propose the hypothesisthat helminth therapy may inhibit the occurrence and development of IBD through inducing immune homeostasis by the proliferation of Treg in gastrointestinal tract. Here we design to investigate the roles of the gastrointestinal tract-specialized regional Tregs induced by TsES and TsPmy during the UC progression, as well as the plasticity and distribution of these Tregs in gut, the relation between these Tregs and intestinal bacteria, and how these Tregs could be recruited to the site attacked by colonic inflammation. We intend to clarify the mechanisms that these Tregs inhibit the occurrence and development of UC. It is expected to greatly add to the theoretical foundation in the interaction between gastrointestinal tract-specialized regional immunologic features and traditional mucosal immune system. Meanwhile, it will further illustrate the molecular mechanism of helminth therapy and provide experimental basis for the development of helminth derived molecules work as immunosuppressor used in target therapy of IBD and other autoimmune diseases.