Abstract
Regulatory T (Treg) cells represent a subpopulation of suppressor CD4+ T cells critically involved in the establishment of peripheral tolerance through the inhibition of effector T (Teff) cells and the suppression of the immune-mediated tissue destruction toward self-antigens. Treg generation, their suppressive properties and also Treg-Teff cell interactions could be modulated at least in part by programmed cell death-1 (PD-1) expression on their surface and through binding between PD-1 and programmed cell death ligand-1 (PD-L1). Defects involving PD-1 and Tregs can lead to the development of pathological conditions, including autoimmune disorders or promote cancer progression by favoring tumor evasion from the host immune response. At the same time, PD-1 and Tregs could represent attractive targets for treatment, as demonstrated by the therapeutic blockade of PD-L1 applied for the management of different cancer conditions in humans. In the present Review, we focus specifically the role of PD-1/PD-L1 on Treg development and activity.
Highlights
The programmed cell death 1 (PD-1, CD80) molecule is a 55kDa type I transmembrane protein [1] belonging to the immunoglobulin superfamily
Murine programmed cell death-1 (PD-1) mRNA expression is associated with activationinduced apoptosis in murine T cell hybridomas, PD-1 binding does not lead to cell death, instead it causes cell cycle blockade
In T1D patients these cells presented reduced percentages of total PD-1+, PD-1low, and PD-1high suggesting that reduced PD-1 expression and a defective PD-1/programmed cell death ligand-1 (PD-L1) signaling pathway could lead to a deficient Treg activation [91]
Summary
The programmed cell death 1 (PD-1, CD80) molecule is a 55kDa type I transmembrane protein [1] belonging to the immunoglobulin superfamily. A moderate lung inflammatory phenotype characterized the lungs of Rag−/− mice administered with anti–PD-L1 mAb. Consistently with the results from PD-L1−/−PD-L2−/− Rag−/− recipients receiving naive CD4 T cells, defective iTreg differentiation as well as pulmonary inflammation develops in wild type Rag−/− mice treated with anti–PD-L1 mAb. Foxp3 expression as well as the suppressive Treg function were increased upon activation of T lymphocytes in presence of PD-L1-Ig [79].
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