Regulation of Neuroinflammation Through Programed Death-1/Programed Death Ligand Signaling in Neurological Disorders

Overview

Journal Front Cell Neurosci

Specialty Cell Biology

Date 2014 Sep 19

PMID 25232304

Citations 26

Authors

Shangfeng Zhao

Fengwu Li

Rehana K Leak

Jun Chen

Xiaoming Hu

Affiliations

Soon will be listed here.

Abstract

Immune responses in the central nervous system (CNS), which involve both resident glial cells and infiltrating peripheral immune cells, play critical roles in the progress of brain injuries and neurodegeneration. To avoid inflammatory damage to the compromised brain, the immune cell activities in the CNS are controlled by a plethora of chemical mediators and signal transduction cascades, such as inhibitory signaling through programed death-1 (PD-1) and programed death ligand (PD-L) interactions. An increasing number of recent studies have highlighted the importance of PD-1/PD-L pathway in immune regulation in CNS disorders such as ischemic stroke, multiple sclerosis, and Alzheimer's disease. Here, we review the current knowledge of the impact of PD-1/PD-L signaling on brain injury and neurodegeneration. An improved understanding of the function of PD-1/PD-L in the cross-talk between peripheral immune cells, CNS glial cells, and non-immune CNS cells is expected to shed further light on immunomodulation and help develop effective and safe immunotherapies for CNS disorders.

Citing Articles

Therapeutic implications for the PD-1 axis in cerebrovascular injury.

Feghali J, Jackson C Neurotherapeutics. 2024; 22(1):e00459.

PMID: 39368872 PMC: 11840351. DOI: 10.1016/j.neurot.2024.e00459.

GM130-silencing may aggravate blood-brain barrier damage and affect microglia polarization by down-regulating PD-L1 expression after experimental intracerebral hemorrhage.

Chen X, Ren Y, Xie P, Lei Q, Lu W Mol Biol Rep. 2024; 51(1):919.

PMID: 39158740 DOI: 10.1007/s11033-024-09859-x.

PD-L1/PD-1 pathway: a potential neuroimmune target for pain relief.

Deng D, Zhang T, Ma L, Zhao W, Huang S, Wang K Cell Biosci. 2024; 14(1):51.

PMID: 38643205 PMC: 11031890. DOI: 10.1186/s13578-024-01227-3.

Endogenous Extracellular Vesicles Participate in Brain Remodeling after Ischemic Stroke.

Muleiro Alvarez M, Esparza Salazar F, Rodriguez T, DEgidio F, Borlongan C, Lee J Int J Mol Sci. 2023; 24(23).

PMID: 38069179 PMC: 10706116. DOI: 10.3390/ijms242316857.

The analgesic effect of programmed cell death protein-1.

Park J Korean J Pain. 2023; 36(2):147-148.

PMID: 36973966 PMC: 10043789. DOI: 10.3344/kjp.23082.

References

Nishimura H, Okazaki T, Tanaka Y, Nakatani K, Hara M, Matsumori A . Autoimmune dilated cardiomyopathy in PD-1 receptor-deficient mice. Science. 2001; 291(5502):319-22. DOI: 10.1126/science.291.5502.319. View

Said E, Dupuy F, Trautmann L, Zhang Y, Shi Y, El-Far M . Programmed death-1-induced interleukin-10 production by monocytes impairs CD4+ T cell activation during HIV infection. Nat Med. 2010; 16(4):452-9. PMC: 4229134. DOI: 10.1038/nm.2106. View

Trabattoni D, Saresella M, Pacei M, Marventano I, Mendozzi L, Rovaris M . Costimulatory pathways in multiple sclerosis: distinctive expression of PD-1 and PD-L1 in patients with different patterns of disease. J Immunol. 2009; 183(8):4984-93. DOI: 10.4049/jimmunol.0901038. View

Carter L, Leach M, Azoitei M, Cui J, Pelker J, Jussif J . PD-1/PD-L1, but not PD-1/PD-L2, interactions regulate the severity of experimental autoimmune encephalomyelitis. J Neuroimmunol. 2006; 182(1-2):124-34. DOI: 10.1016/j.jneuroim.2006.10.006. View

Liesz A, Zhou W, Mracsko E, Karcher S, Bauer H, Schwarting S . Inhibition of lymphocyte trafficking shields the brain against deleterious neuroinflammation after stroke. Brain. 2011; 134(Pt 3):704-20. DOI: 10.1093/brain/awr008. View

Latchman Y, Liang S, Wu Y, Chernova T, Sobel R, Klemm M . PD-L1-deficient mice show that PD-L1 on T cells, antigen-presenting cells, and host tissues negatively regulates T cells. Proc Natl Acad Sci U S A. 2004; 101(29):10691-6. PMC: 489996. DOI: 10.1073/pnas.0307252101. View

Viglietta V, Baecher-Allan C, Weiner H, Hafler D . Loss of functional suppression by CD4+CD25+ regulatory T cells in patients with multiple sclerosis. J Exp Med. 2004; 199(7):971-9. PMC: 2211881. DOI: 10.1084/jem.20031579. View

Brandl C, Ortler S, Herrmann T, Cardell S, Lutz M, Wiendl H . B7-H1-deficiency enhances the potential of tolerogenic dendritic cells by activating CD1d-restricted type II NKT cells. PLoS One. 2010; 5(5):e10800. PMC: 2875405. DOI: 10.1371/journal.pone.0010800. View

Lipp M, Brandt C, Dehghani F, Kwidzinski E, Bechmann I . PD-L1 (B7-H1) regulation in zones of axonal degeneration. Neurosci Lett. 2007; 425(3):156-61. DOI: 10.1016/j.neulet.2007.07.053. View

10.

Li P, Gan Y, Sun B, Zhang F, Lu B, Gao Y . Adoptive regulatory T-cell therapy protects against cerebral ischemia. Ann Neurol. 2013; 74(3):458-71. PMC: 3748165. DOI: 10.1002/ana.23815. View

11.

Zipp F, Aktas O . The brain as a target of inflammation: common pathways link inflammatory and neurodegenerative diseases. Trends Neurosci. 2006; 29(9):518-27. DOI: 10.1016/j.tins.2006.07.006. View

12.

Chang W, Kim J, Kim Y, Kim Y, Lee J, Azuma M . Cutting edge: Programmed death-1/programmed death ligand 1 interaction regulates the induction and maintenance of invariant NKT cell anergy. J Immunol. 2008; 181(10):6707-10. DOI: 10.4049/jimmunol.181.10.6707. View

13.

Liu Y, Zeng F, Wang Y, Zhou H, Giunta B, Tan J . Immunity and Alzheimer's disease: immunological perspectives on the development of novel therapies. Drug Discov Today. 2013; 18(23-24):1212-20. DOI: 10.1016/j.drudis.2013.07.020. View

14.

Koronyo-Hamaoui M, Ko M, Koronyo Y, Azoulay D, Seksenyan A, Kunis G . Attenuation of AD-like neuropathology by harnessing peripheral immune cells: local elevation of IL-10 and MMP-9. J Neurochem. 2009; 111(6):1409-24. DOI: 10.1111/j.1471-4159.2009.06402.x. View

15.

Wang C, Li Y, Proctor T, Vandenbark A, Offner H . Down-modulation of programmed death 1 alters regulatory T cells and promotes experimental autoimmune encephalomyelitis. J Neurosci Res. 2009; 88(1):7-15. PMC: 2783709. DOI: 10.1002/jnr.22181. View

16.

Zhong X, Tumang J, Gao W, Bai C, Rothstein T . PD-L2 expression extends beyond dendritic cells/macrophages to B1 cells enriched for V(H)11/V(H)12 and phosphatidylcholine binding. Eur J Immunol. 2007; 37(9):2405-10. DOI: 10.1002/eji.200737461. View

17.

Kroner A, Mehling M, Hemmer B, Rieckmann P, Toyka K, Maurer M . A PD-1 polymorphism is associated with disease progression in multiple sclerosis. Ann Neurol. 2005; 58(1):50-7. DOI: 10.1002/ana.20514. View

18.

Speciale L, Calabrese E, Saresella M, Tinelli C, Mariani C, Sanvito L . Lymphocyte subset patterns and cytokine production in Alzheimer's disease patients. Neurobiol Aging. 2006; 28(8):1163-9. DOI: 10.1016/j.neurobiolaging.2006.05.020. View

19.

Bodhankar S, Chen Y, Vandenbark A, Murphy S, Offner H . PD-L1 enhances CNS inflammation and infarct volume following experimental stroke in mice in opposition to PD-1. J Neuroinflammation. 2013; 10:111. PMC: 3846120. DOI: 10.1186/1742-2094-10-111. View

20.

Tzartos J, Friese M, Craner M, Palace J, Newcombe J, Esiri M . Interleukin-17 production in central nervous system-infiltrating T cells and glial cells is associated with active disease in multiple sclerosis. Am J Pathol. 2007; 172(1):146-55. PMC: 2189615. DOI: 10.2353/ajpath.2008.070690. View