ArticlePloS one2016
Increased CD86 but Not CD80 and PD-L1 Expression on Liver CD68+ Cells during Chronic HBV Infection.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- The role of liver macrophages in viral liver pathogenesis.Journal of leukocyte biology · 2025Review
- Immunohistochemical Profiling of Immune Checkpoints in Chronic Hepatitis B Liver Tissue.Pathogens (Basel, Switzerland) · 2025Article
- The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions.MedComm · 2025Review
- Characterization of Dendritic Cells and Myeloid-Derived Suppressor Cells Expressing Major Histocompatibility Complex Class II in Secondary Lymphoid Organs in Systemic Lupus Erythematosus-Prone Mice.International journal of molecular sciences · 2024Article
- Insights into Immune Exhaustion in Chronic Hepatitis B: A Review of Checkpoint Receptor Expression.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Review
- Human macrophages and monocyte-derived dendritic cells stimulate the proliferation of endothelial cells through midkine production.PloS one · 2022Article
- The Liver and the Hepatic Immune Response inPathogens (Basel, Switzerland) · 2021Review
- In Vivo and In Vitro Characterization of Primary Human Liver Macrophages and Their Inflammatory State.Biomedicines · 2021Article
- The reduction in CD8BMC infectious diseases · 2020Article
- Human Liver Macrophage Subsets Defined by CD32.Frontiers in immunology · 2020Article
- Pathogenetic Mechanisms of T Cell Dysfunction in Chronic HBV Infection and Related Therapeutic Approaches.Frontiers in immunology · 2020Review
- Chronic Hepatitis C Virus Infection Impairs M1 Macrophage Differentiation and Contributes to CD8Cells · 2019Article
- Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases.Infection and drug resistance · 2019Article
- Recent Findings in the Regulation of Programmed Death Ligand 1 Expression.Frontiers in immunology · 2019Review
- CD80 Regulates Th17 Cell Differentiation in Coxsackie Virus B3-Induced Acute Myocarditis.Inflammation · 2018Article
- The immunological function of extracellular vesicles in hepatitis B virus-infected hepatocytes.PloS one · 2018Article
- CD86 Expression by Monocytes Influences an Immunomodulatory Profile in Asymptomatic Patients with Chronic Chagas Disease.Frontiers in immunology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe failure to establish potent anti-HBV T cell responses suggests the absence of an effective innate immune activation. Kupffer cells and liver-infiltrating monocytes/macrophages have an essential role in establishing anti-HBV responses. These cells express the costimulatory molecules CD80 and CD86. CD80 expression on antigen-presenting cells (APCs) induces Th1 cell differentiation, whereas CD86 expression drives the differentiation towards a Th2 profile. The relative expression of CD80, CD86 and PD-L1 on APCs, regulates T cell activation. Few studies investigated CD80 and CD86 expression on KCs and infiltrating monocytes/macrophages in HBV-infected liver and knowledge about the expression of PD-L1 on these cells is controversial. The expression of these molecules together in CD68+ cells has not been explored in HBV-infected livers.
methodsDouble staining immunohistochemistry was applied to liver biopsies of HBV-infected and control donors to explore CD80, CD86 and PD-L1 expression in the lobular and portal areas.
resultsChronic HBV infection was associated with increased CD68+CD86+ cell count and percentage in the lobular areas, and no changes in the count and percentage of CD68+CD80+ and CD68+PD-L1+ cells, compared to the control group. While CD68+CD80+ cell count in portal areas correlated with the fibrosis score, CD68+CD80+ cell percentage in lobular areas correlated with the inflammation grade.
conclusionThe upregulation of CD86 but not CD80 and PD-L1 on CD68+ cells in HBV-infected livers, suggests that these cells do not support the induction of potent Th1. Moreover, the expression of CD80 on CD68+ cells correlates with liver inflammation and fibrosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.