ArticleJournal for immunotherapy of cancer2026
CD55-expressing myeloid-derived suppressor cells (MDSCs) drive cancer immunoevasion.
Article in Journal for immunotherapy of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyeloid-derived suppressor cells (MDSCs) play a pivotal role in shaping the immunosuppressive tumor microenvironment, thereby driving tumor progression and contributing to resistance to therapy. The surface molecules expressed on MDSCs serve not only as identification markers but also as critical regulators of their immunosuppressive functions. Identifying surface markers that are both widely expressed and functionally significant on MDSCs is essential for the development of effective immunomodulatory therapies.
methodsA comprehensive analysis of publicly available single-cell RNA-seq datasets across eight cancer types was conducted to identify conserved surface markers on MDSCs. CD55 was identified as a promising candidate and subsequently validated in both human patient samples and murine tumor models. Mechanistic investigations employed CD55 knockout and myeloid-specific knockout mice, bone marrow transplantation, DNA pulldown assays, chromatin immunoprecipitation, luciferase reporter assays, co-immunoprecipitation, immunoblotting, immunoprecipitation-mass spectrometry, and RNA sequencing. To evaluate the therapeutic potential of targeting CD55, molecular docking analyses, small-molecule inhibitor screening, and surface plasmon resonance imaging-based competitive binding assays were conducted.
resultsCD55 was consistently overexpressed on MDSCs across multiple cancer types, with its expression correlating with poor patient prognosis. Genetic depletion of CD55 significantly inhibited tumor growth and enhanced antitumor immunity by reducing MDSCs infiltration and boosting CD8
conclusionThis study identified CD55 as a key regulator of MDSCs-mediated tumor immunosuppression via metabolic reprogramming. Targeting CD55 on MDSCs offers a promising therapeutic approach to overcoming immunosuppression and enhancing the efficacy of cancer immunotherapy.
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.