CD4+CD25+ regulatory T-cell deficient mice as a novel mouse model for immune thrombocytopenia

本研究的目的是通过建立一种新的小鼠免疫性血小板减少症(ITP)动物模型，研究Tregs在体内免疫性血小板减少症(ITP)诱导过程中的作用，并根据ITP的病理生理机制开发一种基础治疗方法。我们发现一组Treg缺陷小鼠出现了自身抗体介导的血小板减少症。我们的结果共同表明，CD4^+CD25^+Foxp3^+Tregs在防止小鼠自身抗体介导的血小板减少中发挥了关键作用，这部分是通过CTLA4的作用实现的。

Purposes in this study are to investigate the role of Tregs in the induction phase of immune thrombocytopenia (ITP) in vivo using a novel mouse model and to develop a fundamental treatment based on the pathophysiology of ITP. We have found that a group of Treg-deficient mice develop autoantibody-mediated thrombocytopenia. Our results together indicate that CD4^+ CD25^+ Foxp3^+ Tregs play a critical role in preventing the development of murine autoantibody-mediated thrombocytopenia, in part, through CTLA4 engagement.