ReviewBiomedicines2026
CD86 in Dendritic Cell-Mediated Cancer Immunity: From Maturation Marker to Functional Regulator.
Review in Biomedicines, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Immune modulation in gastric cancer: from macrophage polarization to immunotherapy.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Dendritic cell (DC)-based cancer immunotherapy remains limited by heterogeneous immune responses and variable clinical efficacy. CD86, a key co-stimulatory molecule, is traditionally regarded as a marker of dendritic cell maturation; however, accumulating evidence suggests that CD86 expression is regulated by immune checkpoint interactions, inflammatory signaling, and tumor microenvironment-associated immune modulation. In this review, we summarize current evidence regarding the molecular mechanisms governing CD86 regulation, including MARCH1-mediated ubiquitination and CTLA-4-mediated trans-endocytosis, and discuss how suppressive cytokines, hypoxia, and metabolic stress influence dendritic cell function within the tumor microenvironment (TME). We further review the heterogeneity of CD86 regulation across dendritic cell subsets and immune contexts, as well as its potential relevance in secondary lymphoid organs and tumor-associated immune responses. In addition, we discuss current evidence regarding soluble CD86 (sCD86) and its reported associations with immune activation and dysregulated immune states in cancer. Current evidence supports that CD86 regulation is shaped by integrated co-stimulatory signaling, immune checkpoint interactions, and tumor microenvironment-associated suppression. Importantly, CD86 may function not only as a dendritic cell maturation marker but also as a dynamic immunoregulatory molecule with context-dependent implications in cancer immunity. However, substantial uncertainties remain regarding its mechanistic role, prognostic value, and therapeutic relevance across different tumor settings. Future mechanistic and translational studies are needed to clarify these unresolved issues.
Indexed as
Identifiers
What Socratic 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 Socratic graph.