ArticleApplied immunohistochemistry & molecular morphology : AIMM2017
Modulation of PD-L1 and CD8 Activity in Idiopathic and Infectious Chronic Inflammatory Conditions.
Article in Applied immunohistochemistry & molecular morphology : AIMM, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- A report of two cases of parathyroid adenoma with associated chronic lymphocytic parathyroiditis.JCEM case reports · 2026Article
- Loss of ICOSL expression in the progression to cervical carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Recent advances in the mechanisms of PD-L1 expression in gastric cancer: a review.Biological research · 2025Review
- The influence ofFrontiers in immunology · 2025Article
- Role of PD-L1 in mediating the effect of lipid on ulcerative colitis: a mediation Mendelian randomization study.Frontiers in genetics · 2025Article
- Article
- Causal association between Helicobacter pylori infection and Sjogren's syndrome: a bidirectional Mendelian randomization analysis.BMC infectious diseases · 2024Article
- PD-1-positive cells contribute to the diagnosis of inflammatory bowel disease and can aid in predicting response to vedolizumab.Scientific reports · 2023Article
- The differential immune response in mild versus fatal SARS-CoV2 infection.Annals of diagnostic pathology · 2022Article
- Beyond Cancer: Regulation and Function of PD-L1 in Health and Immune-Related Diseases.International journal of molecular sciences · 2022Review
- Review
- Helicobacter pylori and its association with autoimmune diseases: systemic lupus erythematosus, rheumatoid arthritis and Sjögren syndrome.Journal of translational autoimmunity · 2021Article
- Role of PD-L1 in Gut Mucosa Tolerance and Chronic Inflammation.International journal of molecular sciences · 2020Review
- PD-L1 expression and survival in p16-negative and -positive squamous cell carcinomas of the vulva.Journal of cancer research and clinical oncology · 2020Article
- JAK Inhibitors and Oxidative Stress Control.Frontiers in immunology · 2019Article
- RNA-sequencing in non-small cell lung cancer shows gene downregulation of therapeutic targets in tumor tissue compared to non-malignant lung tissue.Radiation oncology (London, England) · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Programmed death-ligand 1 (PD-L1) can reduce the immune response by inhibiting CD8 T-cell proliferation and cytotoxic activity. We studied a series of human viral (molloscum, human papillomavirus, herpes simplex, cytomegalovirus, Epstein-Barr virus, smallpox) and bacterial infections (Helicobacter pylori) for the in situ expression of PD-L1, mononuclear cell infiltration, and CD8 activity and compared this to noninfectious idiopathic inflammatory conditions to better define which immune responses may be more highly correlated with an infectious agent. Each viral and bacterial infection showed an increased PD-L1 expression that was most prominent in the mononuclear cell/CD8+ infiltrate surrounding the infection. However, the CD8 cells were mostly quiescent as evidenced by the low Ki67 index and minimal granzyme expression. Using a melanoma mouse model, acute reovirus infection increased PD-L1 expression, but decreased CD8 cytotoxic activity and Treg (FOXP3) cell numbers. In comparison, idiopathic noninfectious chronic inflammatory processes including lichen sclerosis, eczema, Sjogren's disease, and ulcerative colitis showed a comparable strong PD-L1 expression in the mononuclear cell infiltrates but much greater Treg infiltration. However, this strong immunosuppressor profile was ineffective as evidenced by strong CD8 proliferation and granzyme expression. These data suggest that viral and bacterial infections induce a PD-L1 response that, unlike noninfectious chronic inflammatory conditions, dampens the activity of the recruited CD8 cells which, in turn, may enhance the ability of anti-PD-L1 therapy to eliminate the infectious agent.
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