ReviewFrontiers in immunology2016
Autosomal Minor Histocompatibility Antigens: How Genetic Variants Create Diversity in Immune Targets.
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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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
57 citing papers in PubMed, 82 citations in OpenAlex.
- Trial
- Minor histocompatibility antigen TCR-T.Blood advances · 2026Review
- HLA-AJournal of immunology research · 2026Article
- Framework for predicting alloreactivity in hematopoietic cell transplants.Nature biotechnology · 2025Article
- Systematic identification of minor histocompatibility antigens predicts outcomes of allogeneic hematopoietic cell transplantation.Nature biotechnology · 2025Article
- DNA barcoded peptide-MHC multimers to measure and monitor minor histocompatibility antigen-specific T cells after allogeneic stem cell transplantation.Journal for immunotherapy of cancer · 2024Article
- Article
- Tissue-specific features of the T cell repertoire after allogeneic hematopoietic cell transplantation in human and mouse.Science translational medicine · 2023Article
- Shared graft-versus-leukemia minor histocompatibility antigens in DISCOVeRY-BMT.Blood advances · 2023Article
- Immunology of cord blood T-cells favors augmented disease response during clinical pediatric stem cell transplantation for acute leukemia.Frontiers in pediatrics · 2023Review
- An unexplored angle: T cell antigen discoveries reveal a marginal contribution of proteasome splicing to the immunogenic MHC class I antigen pool.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Allogeneic MHC-matched T-cell receptor α/β-depleted bone marrow transplants in SHIV-infected, ART-suppressed Mauritian cynomolgus macaques.Scientific reports · 2022Article
- Engineered cellular immunotherapies in cancer and beyond.Nature medicine · 2022Review
- Immune Editing: Overcoming Immune Barriers in Stem Cell Transplantation.Current stem cell reports · 2022Review
- Targeted minor histocompatibility antigen typing to estimate graft-versus-host disease after allogeneic haematopoietic stem cell transplantation.Bone marrow transplantation · 2021Article
- Article
- 60 Years Young: The Evolving Role of Allogeneic Hematopoietic Stem Cell Transplantation in Cancer Immunotherapy.Cancer research · 2021Review
- Genetics of HLA Peptide Presentation and Impact on Outcomes in HLA-Matched Allogeneic Hematopoietic Cell Transplantation.Transplantation and cellular therapy · 2021Article
- Self-Peptidome Variation Shapes Individual Immune Responses.Trends in genetics : TIG · 2021Review
- Mouse Models of Antigen Presentation in Hematopoietic Stem Cell Transplantation.Frontiers in immunology · 2021Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allogeneic stem cell transplantation (alloSCT) can be a curative treatment for hematological malignancies. Unfortunately, the desired anti-tumor or graft-versus-leukemia (GvL) effect is often accompanied with undesired side effects against healthy tissues known as graft-versus-host disease (GvHD). After HLA-matched alloSCT, GvL and GvHD are both mediated by donor-derived T-cells recognizing polymorphic peptides presented by HLA surface molecules on patient cells. These polymorphic peptides or minor histocompatibility antigens (MiHA) are produced by genetic differences between patient and donor. Since polymorphic peptides may be useful targets to manipulate the balance between GvL and GvHD, the dominant repertoire of MiHA needs to be discovered. In this review, the diversity of autosomal MiHA characterized thus far as well as the various molecular mechanisms by which genetic variants create immune targets and the role of cryptic transcripts and proteins as antigen sources are described. The tissue distribution of MiHA as important factor in GvL and GvHD is considered as well as possibilities how hematopoietic MiHA can be used for immunotherapy to augment GvL after alloSCT. Although more MiHA are still needed for comprehensive understanding of the biology of GvL and GvHD and manipulation by immunotherapy, this review shows insight into the composition and kinetics of in vivo immune responses with respect to specificity, diversity, and frequency of specific T-cells and surface expression of HLA-peptide complexes and other (accessory) molecules on the target cell. A complex interplay between these factors and their environment ultimately determines the spectrum of clinical manifestations caused by immune responses after alloSCT.
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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.