PD-L1 regulates the development, maintenance, and function of induced regulatory T cells

Journal of Experimental Medicine - Tập 206 Số 13 - Trang 3015-3029 - 2009
Loise M. Francisco1,2,3, Victor H. Salinas4, Keturah Brown3, Vijay K. Vanguri1,2,3, Gordon J. Freeman5, Vijay K. Kuchroo1,2, Arlene H. Sharpe1,2,3
1Center for Neurological Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115 2 and 3
2Department of Pathology and Center for Neurological Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115
3Department of Pathology, Harvard Medical School, Boston, MA 02115 1
4Harvard University, Cambridge, MA 02138 4
5Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115 5

Tóm tắt

Both the programmed death (PD) 1–PD-ligand (PD-L) pathway and regulatory T (T reg) cells are instrumental to the maintenance of peripheral tolerance. We demonstrate that PD-L1 has a pivotal role in regulating induced T reg (iT reg) cell development and sustaining iT reg cell function. PD-L1−/− antigen-presenting cells minimally convert naive CD4 T cells to iT reg cells, showing the essential role of PD-L1 for iT reg cell induction. PD-L1–coated beads induce iT reg cells in vitro, indicating that PD-L1 itself regulates iT reg cell development. Furthermore, PD-L1 enhances and sustains Foxp3 expression and the suppressive function of iT reg cells. The obligatory role for PD-L1 in controlling iT reg cell development and function in vivo is illustrated by a marked reduction in iT reg cell conversion and rapid onset of a fatal inflammatory phenotype in PD-L1−/−PD-L2−/− Rag−/− recipients of naive CD4 T cells. PD-L1 iT reg cell development is mediated through the down-regulation of phospho-Akt, mTOR, S6, and ERK2 and concomitant with the up-regulation of PTEN, all key signaling molecules which are critical for iT reg cell development. Thus, PD-L1 can inhibit T cell responses by promoting both the induction and maintenance of iT reg cells. These studies define a novel mechanism for iT reg cell development and function, as well as a new strategy for controlling T reg cell plasticity.

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