ReviewJournal of immunology research2026
HLA-G in Hematological Malignancies: Immunoregulatory Mechanisms and Implications for Immune Evasion and Immunotherapy.
Review in Journal of immunology research, 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.
- HLA-G in Hematological Malignancies: Immunoregulatory Mechanisms and Implications for Immune Evasion and Immunotherapy.Journal of immunology research · 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
12 authors.
Funding
Abstract
Human leukocyte antigen G (HLA-G) is a nonclassical major histocompatibility complex class I molecule whose increased expression has been consistently associated with unfavorable prognosis in solid tumors and has emerged as a potential immunotherapeutic target in hematological malignancies. HLA-G exhibits limited genetic diversity and generates multiple isoforms that play a critical role in immune tolerance, being physiologically expressed in immunoprivileged tissues and aberrantly upregulated in a variety of pathological conditions, including cancer. Accumulating evidence indicates that elevated HLA-G expression contributes to tumor immune evasion and influences clinical outcomes in patients with leukemia, lymphoma, and multiple myeloma. Genetic variability within the HLA-G gene, particularly polymorphisms located in regulatory regions such as the 14-base pair insertion/deletion, has been associated with cancer susceptibility, disease progression, and adverse prognosis. In hematological malignancies, specific genotypes, including the homozygous deletion variant, have been linked to increased levels of membrane-bound and soluble HLA-G, correlating with impaired immune surveillance and reduced survival, particularly in chronic lymphocytic leukemia. Moreover, HLA-G expressions may be modulated by inflammatory cytokines, such as interferon-γ, further shaping the immunosuppressive tumor microenvironment. By functioning as a nonclassical immune checkpoint, HLA-G represents a promising target for innovative immunotherapeutic strategies, including immune checkpoint blockade combinations and chimeric antigen receptor (CAR)-T cell approaches directed against HLA-G-expressing malignant cells. In this review, we summarize current knowledge regarding HLA-G expression, genetic polymorphisms, and immunoregulatory mechanisms in hematological malignancies, highlighting their clinical and translational implications. Improved understanding of HLA-G-mediated immune modulation may contribute to the development of novel prognostic biomarkers and therapeutic strategies aimed at restoring effective antitumor immunity.
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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.