ArticleThe American journal of pathology2009
Accelerated course of experimental autoimmune encephalomyelitis in PD-1-deficient central nervous system myelin mutants.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Neurological Immune-Related Adverse Events Induced by Immune Checkpoint Inhibitors.Biomedicines · 2024Review
- Frequency of demyelinating disease activity following immune checkpoint inhibitor cancer immunotherapy.Journal of neurology · 2023Article
- Selective ablation of thymic and peripheral Foxp3Frontiers in immunology · 2023Article
- Regulation of the programmed cell death protein 1/programmed cell death ligand 1 axis in relapsing-remitting multiple sclerosis.Brain communications · 2023Article
- PD-1/PD-L Axis in Neuroinflammation: New Insights.Frontiers in neurology · 2022Review
- Drug-related immune-mediated myelopathies.Frontiers in neurology · 2022Review
- Regulation of autoreactive CD4 T cells by FoxO1 signaling in CNS autoimmunity.Journal of neuroimmunology · 2021Article
- PD-1 restraint of regulatory T cell suppressive activity is critical for immune tolerance.The Journal of experimental medicine · 2021Article
- Paraneoplastic Neurological Syndromes and Beyond Emerging With the Introduction of Immune Checkpoint Inhibitor Cancer Immunotherapy.Frontiers in neurology · 2021Review
- Immune Checkpoint Inhibitors and Neurotoxicity.Current neuropharmacology · 2021Review
- Durvalumab and multiple sclerosis: a causal link or simple unmasking?European journal of clinical pharmacology · 2020Article
- Developmental Exposure to a Mixture of 23 Chemicals Associated With Unconventional Oil and Gas Operations Alters the Immune System of Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Inflammatory CNS disease caused by immune checkpoint inhibitors: status and perspectives.Nature reviews. Neurology · 2017Review
- Maintenance of PD-1 on brain-resident memory CD8 T cells is antigen independent.Immunology and cell biology · 2017Article
- Regulation of effector function of CNS autoreactive CD4 T cells through inhibitory receptors and IL-7Rα.Journal of neuroinflammation · 2016Article
- B7-H1 shapes T-cell-mediated brain endothelial cell dysfunction and regional encephalitogenicity in spontaneous CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Inflammation, Iron, Energy Failure, and Oxidative Stress in the Pathogenesis of Multiple Sclerosis.Oxidative medicine and cellular longevity · 2015Review
- The importance of mouse models to define immunovirologic determinants of progressive multifocal leukoencephalopathy.Frontiers in immunology · 2014Review
- Programmed cell death 1 inhibits inflammatory helper T-cell development through controlling the innate immune response.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- PD-1 Interaction with PD-L1 but not PD-L2 on B-cells Mediates Protective Effects of Estrogen against EAE.Journal of clinical & cellular immunology · 2013Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is assumed that the onset and course of autoimmune inflammatory central nervous system (CNS) disorders (eg, multiple sclerosis) are influenced by factors that afflict immune regulation as well as CNS vulnerability. We challenged this concept experimentally by investigating how genetic alterations that affect myelin (primary oligodendrocyte damage in PLPtg mice) and/or T-cell regulation (deficiency of PD-1) influence both the onset and course of an experimental autoimmune CNS inflammatory disease [MOG(35-55)-induced experimental autoimmune encephalomyelitis (EAE)]. We observed that double pathology was associated with a significantly earlier onset of disease, a slight increase in the neurological score, an increase in the number of infiltrating cells, and enhanced axonal degeneration compared with wild-type mice and the respective, single mutant controls. Double-mutant PLPtg/PD-1(-/-) mice showed an increased production of interferon-gamma by CNS immune cells at the peak of disease. Neither PD-1 deficiency nor oligodendropathy led to detectable spread of antigenic MHC class I- or class II-restricted epitopes during EAE. However, absence of PD-1 clearly increased the propensity of T lymphocytes to expand, and the number of clonal expansions reliably reflected the severity of the EAE disease course. Our data show that the interplay between immune dysregulation and myelinopathy results in a stable exacerbation of actively induced autoimmune CNS inflammation, suggesting that the combination of several pathological issues contributes significantly to disease susceptibility or relapses in human disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.