Evaluating the clinical preparation of physician assistant versus nurse practitioner students and the characteristics of their preceptors

Abstract

CD4+Foxp3+ regulatory T cells (Tregs) and antigen presenting cells (APCs) play an important role in maintaining peripheral tolerance but are otherwise exploited by tumors to create a state of unresponsiveness towards tumor antigens. The mechanisms of Treg mediated suppression are sti~l not well understood. This work seeks to elucidate the role of major histocompatibility complex class II (MHC-II) dependent events in CD4+Foxp3+ Treg mediated .suppression. The studies described here take advantage of novel conditional MHC-II deficient mice, which lack expression of MHC-II on peripheral APCs but still maintain their own naYve CD4 T cells and Tregs. In an in vitro system antigen-specific Tregs suppress CD8 T cell proliferation and effector molecule production in an antigen-specific and MHC-II dependent manner. In vivo, MHC-II deficiency resulted in a delay in tumor progression that was CD8 T cell dependent. We further describe two in vivo models in which the role of MHC-II dependent events in Treg mediated suppression can be tested. Therefore, a better understanding of Treg mediated suppression in the context of tumor-induced tolerance could provide potential strategies that could be utilized for anti-tumor immunotherapy.