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. 2019 Apr 4;20(7):1677. doi: 10.3390/ijms20071677

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Glial cell modulation of T lymphocytes via the programmed death (PD)-1: PD-L1 pathway. (A) Engagement of the PD-1 receptor by its ligand PD-L1 results in functional suppression of brain-infiltrating T-cells. This results in controlled neuroinflammation, suppression of disease severity, and limited bystander tissue damage, but may also support persistent viral infection. (B) Blocking the PD-1: PD-L1 negative checkpoint results in the attack of infected glia by effector T-cells resulting in rapid viral clearance, but it may also promote reactive gliosis, exacerbated neuroinflammation, and disease severity. represents blocking either PD-1 or PD-L1 using inhibitors; indicates blocking the PD-1: PD-L1 pathway; engagement of PD-1 to PD-L1; binding of major histocompatibility complex-antigen (MHC-Ag) to T-cell receptor (TCR).

Inline graphic — Glial cell modulation of T lymphocytes via the programmed death (PD)-1: PD-L1 pathway. (A) Engagement of the PD-1 receptor by its ligand PD-L1 results in functional suppression of brain-infiltrating T-cells. This results in controlled neuroinflammation, suppression of disease severity, and limited bystander tissue damage, but may also support persistent viral infection. (B) Blocking the PD-1: PD-L1 negative checkpoint results in the attack of infected glia by effector T-cells resulting in rapid viral clearance, but it may also promote reactive gliosis, exacerbated neuroinflammation, and disease severity. represents blocking either PD-1 or PD-L1 using inhibitors; indicates blocking the PD-1: PD-L1 pathway; engagement of PD-1 to PD-L1; binding of major histocompatibility complex-antigen (MHC-Ag) to T-cell receptor (TCR).