Evidence map›Paper›PMID 31379830›Full record

ArticleFrontiers in immunology2019

Computational Analysis of HLA-presentation of Non-synonymous Recipient Mismatches Indicates Effect on the Risk of Chronic Graft-vs.-Host Disease After Allogeneic HSCT.

Jarmo Ritari, Kati Hyvärinen, Satu Koskela, Riitta Niittyvuopio, Anne Nihtinen, Urpu Salmenniemi, Mervi Putkonen, Liisa Volin, Tony Kwan, Tomi Pastinen and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 2 pooled it
0.7field-weighted citation impact, top 31% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 3 countries.

Jarmo RitariFinnish Red Cross Blood Service, Helsinki, Finland.
Kati HyvärinenFinnish Red Cross Blood Service, Helsinki, Finland.
Satu KoskelaFinnish Red Cross Blood Service, Helsinki, Finland.
Riitta NiittyvuopioStem Cell Transplantation Unit, Department of Hematology, Comprehensive Cancer Center, Helsinki University Hospital, Helsinki, Finland.
Anne NihtinenStem Cell Transplantation Unit, Department of Hematology, Comprehensive Cancer Center, Helsinki University Hospital, Helsinki, Finland.
Urpu SalmenniemiStem Cell Transplantation Unit, Division of Medicine, Department of Hematology, Turku University Hospital, Turku, Finland.
Mervi PutkonenStem Cell Transplantation Unit, Division of Medicine, Department of Hematology, Turku University Hospital, Turku, Finland.
Liisa VolinStem Cell Transplantation Unit, Department of Hematology, Comprehensive Cancer Center, Helsinki University Hospital, Helsinki, Finland.
Tony KwanDepartment of Human Genetics, McGill University and Genome Quebec Innovation Centre, McGill University, Montreal, QC, Canada.
Tomi PastinenDepartment of Human Genetics, McGill University and Genome Quebec Innovation Centre, McGill University, Montreal, QC, Canada.
Maija Itälä-RemesStem Cell Transplantation Unit, Division of Medicine, Department of Hematology, Turku University Hospital, Turku, Finland.
Jukka PartanenFinnish Red Cross Blood Service, Helsinki, Finland.
Finnish Red Cross · FIHelsinki University Hospital · FITurku University Hospital · FIMcGill Genome Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic mismatches in protein coding genes between allogeneic hematopoietic stem cell transplantation (allo-HSCT) recipient and donor can elicit an alloimmunity response via peptides presented by the recipient HLA receptors as minor histocompatibility antigens (mHAs). While the impact of individual mHAs on allo-HSCT outcome such as graft-vs.-host and graft-vs.-leukemia effects has been demonstrated, it is likely that established mHAs constitute only a small fraction of all immunogenic non-synonymous variants. In the present study, we have analyzed the genetic mismatching in 157 exome-sequenced sibling allo-HSCT pairs to evaluate the significance of polymorphic HLA class I associated peptides on clinical outcome. We applied computational mismatch estimation approaches based on experimentally verified HLA ligands available in public repositories, published mHAs, and predicted HLA-peptide affinites, and analyzed their associations with chronic graft-vs.-host disease (cGvHD) grades. We found that higher estimated recipient mismatching consistently increased the risk of severe cGvHD, suggesting that HLA-presented mismatching influences the likelihood of long-term complications in the patient. Furthermore, computational approaches focusing on estimation of HLA-presentation instead of all non-synonymous mismatches indiscriminately may be beneficial for analysis sensitivity and could help identify novel mHAs.

Indexed as

GenotypeGraft vs Host DiseaseGraft vs Leukemia EffectHematopoietic Stem Cell TransplantationHistocompatibilityHistocompatibility TestingHumansMinor Histocompatibility AntigensSiblingsTissue DonorsTransplantation, HomologousMinor Histocompatibility Antigensgenomicsgraft-vs.-hostHLAHSCTminor histocompatibility antigenwhole-exome sequencing

Identifiers

PMID31379830
PMCPMC6646417
OpenAlexW2959732965

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.