Excretory-Secretory Products Stimulate Host Regulatory T Cell Differentiation through Activating Dendritic Cells.

maintains chronic infections within its host, involving a variety of immunomodulatory properties, the mechanisms of which have not been completely elucidated. In this study, we found that infection induced strong regulatory T cell responses through parasite excretory-secretory (ES) products, characterized by increase of CD4CD25Foxp3 and CD4CD25Foxp3 Treg cells accompanied by high levels of IL-10 and TGF-β. adult worm excretory-secretory products (AES) and muscle larvae excretory-secretory products (MES) were both able to activate BMDCs in vitro to facilitate their maturation and to create regulatory cytokines IL-10 and TGF-β. The T AES- and MES-pulsed dendritic cells (DCs) possessed abilities not only to present antigens to sensitized CD4 T cell to stimulate their proliferation but also to induce naive CD4 T cells to differentiate to Treg cells secreting IL-10 and TGF-β. The passive transfer of AES- and MES-pulsed bone marrow-derived dendritic cells (BMDCs) conferred the naive mice to acquire the differentiation of Treg cells. AES possesses a better ability to induce Treg cells than did MES, although the latter has the ability to induce CD4CD25Foxp3 Treg cells. The results obtained in this study suggested that ES products stimulate the differentiation of host Treg cells possibly through activating dendritic cells to create a regulatory environment that benefits the survival of the parasite in the host.