特异性免疫耐受干预是针对过敏性疾病和自身免疫性疾病的理想手段，但特异性耐受的体内机制是瓶颈问题。本实验室曾发现一种诱导特异性耐受的新疫苗，“共免疫”疫苗。此疫苗诱导机体产生CD25阴性iTreg细胞（CD25- iTreg cells），从而产生特异性免疫耐受达到抑制或治疗疾病作用。但此细胞如何在体内产生抗原特异性耐受的机制不清楚，所以本项目针对“共免疫”疫苗诱导特异性耐受的体内作用机制这一科学问题，提出疫苗诱导的抗原特异性 iTreg 在引流淋巴结中建立诱捕点，捕获和缴械炎症T细胞，从而建立特异性免疫耐受的假说。通过研究此iTreg在体内的作用位点、归巢定位机制、对位点微环境的重构、对炎症T细胞的诱捕、及对诱捕到的炎症T细胞进行抑制或使其无能，探明此疫苗诱导特异性免疫耐受的新型免疫诱捕理论。该假说如果能被证实，将对特异性免疫耐受机理研究、自身免疫性疾病的耐受疫苗开发提供理论基础。

Antigen specific treatment of allergy and autoimmune disease has been proposed but still is challenging due to unclear mechanism in vivo. Recently we discovered a novel vaccine called "Co-immunization Vaccine" inducing regulatory T cells. Co-immunization Vaccine induces antigen-specific Treg in vivo, suppressing inflammation in animal models of allergic asthma, allergic dermatitis and type 1 diabetes, in antigen specific manner. Therefore, this vaccine can be called as "Toleragenic Vaccine". To elucidate its suppressive mechanism in vivo, based on our preliminary data, we propose a "Immune Cell Entrapment" hypothesis, which is "CD25 negative iTreg induced by Co-immunization Vaccine set up a trap in draining lymph node with Ag specific APC to lure, trap and eliminate disease causing T cells". To test this hypothesis, we will investigate 1) suppressive locations and, homing regulations of the CD25 negative iTreg; 2) changes of microenvironment by the CD25 negative iTreg; 3) entrapment and elimination of the inflamed T cells, in an antigen specific asthma model. These results will fill our knowledge gap between the mechanism inhibitions of iTreg in vitro from in vivo, and will break a new ground for the antigen specific tolerance treatment against allergic and autoimmune diseases with the toleragenic vaccination approach.