ArticlePloS one2011
Common minor histocompatibility antigen discovery based upon patient clinical outcomes and genomic data.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Minor histocompatibility antigen TCR-T.Blood advances · 2026Review
- CD3 downregulation identifies high-avidity human CD8 T cells.Clinical and experimental immunology · 2024Article
- Associations of minor histocompatibility antigens with outcomes following allogeneic hematopoietic cell transplantation.American journal of hematology · 2023Article
- 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
- Genetics of HLA Peptide Presentation and Impact on Outcomes in HLA-Matched Allogeneic Hematopoietic Cell Transplantation.Transplantation and cellular therapy · 2021Article
- Rapid Multiplex Genotyping of 20 HLA-AFrontiers in immunology · 2019Article
- Computational modeling and confirmation of leukemia-associated minor histocompatibility antigens.Blood advances · 2018Article
- Article
- Determining the Quantitative Principles of T Cell Response to Antigenic Disparity in Stem Cell Transplantation.Frontiers in immunology · 2018Review
- Sequence homology between HLA-bound cytomegalovirus and human peptides: A potential trigger for alloreactivity.PloS one · 2017Article
- Minor histocompatibility Ags: identification strategies, clinical results and translational perspectives.Bone marrow transplantation · 2016Review
- Autosomal Minor Histocompatibility Antigens: How Genetic Variants Create Diversity in Immune Targets.Frontiers in immunology · 2016Review
- Role of Pharmacogenetics in Hematopoietic Stem Cell Transplantation Outcome in Children.International journal of molecular sciences · 2015Review
- Peptide/MHC tetramer-based sorting of CD8⁺ T cells to a leukemia antigen yields clonotypes drawn nonspecifically from an underlying restricted repertoire.Cancer immunology research · 2015Article
- Adoptive T-cell therapy for Leukemia.Molecular and cellular therapies · 2014Review
- In silico Derivation of HLA-Specific Alloreactivity Potential from Whole Exome Sequencing of Stem-Cell Transplant Donors and Recipients: Understanding the Quantitative Immunobiology of Allogeneic Transplantation.Frontiers in immunology · 2014Review
- Augmentation of anti-tumor immunity by adoptive T-cell transfer after allogeneic hematopoietic stem cell transplantation.Expert review of hematology · 2012Review
- The delicate balance of graft versus leukemia and graft versus host disease after allogeneic hematopoietic stem cell transplantation.Expert review of hematologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundMinor histocompatibility antigens (mHA) mediate much of the graft vs. leukemia (GvL) effect and graft vs. host disease (GvHD) in patients who undergo allogeneic stem cell transplantation (SCT). Therapeutic decision making and treatments based upon mHAs will require the evaluation of multiple candidate mHAs and the selection of those with the potential to have the greatest impact on clinical outcomes. We hypothesized that common, immunodominant mHAs, which are presented by HLA-A, B, and C molecules, can mediate clinically significant GvL and/or GvHD, and that these mHAs can be identified through association of genomic data with clinical outcomes. METHODOLOGY/PRINCIPAL
findingsBecause most mHAs result from donor/recipient cSNP disparities, we genotyped 57 myeloid leukemia patients and their donors at 13,917 cSNPs. We correlated the frequency of genetically predicted mHA disparities with clinical evidence of an immune response and then computationally screened all peptides mapping to the highly associated cSNPs for their ability to bind to HLA molecules. As proof-of-concept, we analyzed one predicted antigen, T4A, whose mHA mismatch trended towards improved overall and disease free survival in our cohort. T4A mHA mismatches occurred at the maximum theoretical frequency for any given SCT. T4A-specific CD8+ T lymphocytes (CTLs) were detected in 3 of 4 evaluable post-transplant patients predicted to have a T4A mismatch. CONCLUSIONS/SIGNIFICANCE: Our method is the first to combine clinical outcomes data with genomics and bioinformatics methods to predict and confirm a mHA. Refinement of this method should enable the discovery of clinically relevant mHAs in the majority of transplant patients and possibly lead to novel immunotherapeutics.
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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.