Evidence map›Paper›PMID 42001947›Full record

ArticleThe Journal of biological chemistry2026

Allelic variation alters expression and antigen presentation of MR1 allomorphs.

Adam G Nelson, Victoria Letoga, Clarice Z Q Lee, Carolyn Samer, Songyi Li, Lucy J Meehan, Hamish E G McWilliam, Nicholas A Gherardin, Allison Abendroth, Jose A Villadangos and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

17 authors.

Adam G NelsonDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia.
Victoria LetogaDepartment of Biochemistry and Molecular Biology, Immunity Program, Biomedicine Discovery Institute, Monash University, Victoria, Australia.
Clarice Z Q LeeDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia.
Carolyn SamerInfection, Immunity and Inflammation, School of Medical Sciences, Faculty of Medicine and Health, and the Charles Perkins Centre and Sydney Institute of Infectious Diseases, The University of Sydney, Camperdown, New South Wales, Australia.
Songyi LiDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia.
Lucy J MeehanDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia.
Hamish E G McWilliamDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia; Department of Biochemistry and Pharmacology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Victoria, Australia.
Nicholas A GherardinDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia.
Allison AbendrothInfection, Immunity and Inflammation, School of Medical Sciences, Faculty of Medicine and Health, and the Charles Perkins Centre and Sydney Institute of Infectious Diseases, The University of Sydney, Camperdown, New South Wales, Australia.
Jose A VilladangosDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia; Department of Biochemistry and Pharmacology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Victoria, Australia.
Barry SlobedmanInfection, Immunity and Inflammation, School of Medical Sciences, Faculty of Medicine and Health, and the Charles Perkins Centre and Sydney Institute of Infectious Diseases, The University of Sydney, Camperdown, New South Wales, Australia.
Alexandra J CorbettDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia.
James McCluskeyDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia.
Jamie RossjohnDepartment of Biochemistry and Molecular Biology, Immunity Program, Biomedicine Discovery Institute, Monash University, Victoria, Australia; Institute of Infection and Immunity, Cardiff University, School of Medicine, Cardiff, United Kingdom.
Zhenjun ChenDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia.
Michael N T SouterDepartment of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Victoria, Australia. Electronic address: michael.souter@unimelb.edu.au.
Wael AwadDepartment of Biochemistry and Molecular Biology, Immunity Program, Biomedicine Discovery Institute, Monash University, Victoria, Australia. Electronic address: wael.awad@monash.edu.

Funding

Investigating the basis of MAIT cell antigen potencyR01AI148407 · NIAID · UNIVERSITY OF MELBOURNE · PI MCCLUSKEY, JAMES · 2020 to 2024
$2.7M
NIAID NIH HHS R01 AI148407
6 · The paper itself

Abstract

The major histocompatibility complex (MHC) class I-related protein 1 (MR1) presents vitamin B-derived metabolites to mucosal-associated invariant T (MAIT) and other T cells. There is limited polymorphism of MR1, the functional impact of which is not understood. We examined the impact of allelic variation of MR1 on the expression, structure and function of the known MR1 allomorphs. The expression and function of MR1∗02, MR1∗03, and MR1∗06 were similar to the canonical MR1∗01. Crystal structures of four MR1 allomorphs show that their polymorphisms do not impact the three-dimensional fold of MR1. Despite the binding of 5-OP-RU to MR1∗05 and its cell surface upregulation, this allomorph was severely impaired in its ability to activate primary MAIT cells. This phenotype was controlled by two (His90Gln and Glu52Gly) of its three polymorphisms, which led to the loss of structurally stabilizing interactions. When cells expressing the MR1 allomorphs were infected with herpes simplex virus type 1 (HSV-1), the nascent expression of all allomorphs was severely impaired, but surface expression of MR1∗04:01 and MR1∗04:02 was relatively less impacted. Hence, MR1 allelic variation alters the expression and function of the MR1∗04 and MR1∗05 allomorphs, with implications for MAIT cell and diverse MR1-reactive T cell immunity.

Indexed as

AllelesAntigen PresentationHistocompatibility Antigens Class IMinor Histocompatibility AntigensAnimalsHumansMucosal-Associated Invariant T CellsPolymorphism, GeneticHistocompatibility Antigens Class IMinor Histocompatibility AntigensMR1 protein, humanalleleantigenMAITMR1polymorphism

Identifiers

PMID42001947
PMCPMC13213668

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Registered trials

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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.