Evidence map›Paper›PMID 27534821›Full record

ReviewOpen biology2016

Human leukocyte Antigen-DM polymorphisms in autoimmune diseases.

Miguel Alvaro-Benito, Eliot Morrison, Marek Wieczorek, Jana Sticht, Christian Freund

Open access · goldAbstract readReview
In one paragraph

Review in Open biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  7. Sortase-Mediated Multi-Fragment Assemblies by Ligation Site Switching.Angewandte Chemie (International ed. in English) · 2022
    Article
  8. Review
  9. Subacute combined degeneration of the spinal cord with concomitant autoimmune disease: report of 2 cases.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Article
  10. Article
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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

5 authors at 1 institution in 2 countries.

Miguel Alvaro-BenitoProtein Biochemistry Group, Institute for Chemistry and Biochemistry, Department of Biology, Chemistry and Pharmacy, Freie Universität Berlin, Berlin, Germany malvaro@zedat.fu-berlin.de.ORCID 0000-0002-6019-3567
Eliot MorrisonProtein Biochemistry Group, Institute for Chemistry and Biochemistry, Department of Biology, Chemistry and Pharmacy, Freie Universität Berlin, Berlin, Germany.
Marek WieczorekProtein Biochemistry Group, Institute for Chemistry and Biochemistry, Department of Biology, Chemistry and Pharmacy, Freie Universität Berlin, Berlin, Germany.
Jana StichtProtein Biochemistry Group, Institute for Chemistry and Biochemistry, Department of Biology, Chemistry and Pharmacy, Freie Universität Berlin, Berlin, Germany.
Christian FreundProtein Biochemistry Group, Institute for Chemistry and Biochemistry, Department of Biology, Chemistry and Pharmacy, Freie Universität Berlin, Berlin, Germany chfreund@zedat.fu-berlin.de.
Google (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Classical MHC class II (MHCII) proteins present peptides for CD4(+) T-cell surveillance and are by far the most prominent risk factor for a number of autoimmune disorders. To date, many studies have shown that this link between particular MHCII alleles and disease depends on the MHCII's particular ability to bind and present certain peptides in specific physiological contexts. However, less attention has been paid to the non-classical MHCII molecule human leucocyte antigen-DM, which catalyses peptide exchange on classical MHCII proteins acting as a peptide editor. DM function impacts the presentation of both antigenic peptides in the periphery and key self-peptides during T-cell development in the thymus. In this way, DM activity directly influences the response to pathogens, as well as mechanisms of self-tolerance acquisition. While decreased DM editing of particular MHCII proteins has been proposed to be related to autoimmune disorders, no experimental evidence for different DM catalytic properties had been reported until recently. Biochemical and structural investigations, together with new animal models of loss of DM activity, have provided an attractive foundation for identifying different catalytic efficiencies for DM allotypes. Here, we revisit the current knowledge of DM function and discuss how DM function may impart autoimmunity at the organism level.

Indexed as

Polymorphism, Single NucleotideAnimalsAntigen PresentationAutoimmune DiseasesGene EditingGenetic Predisposition to DiseaseHLA-D AntigensHumansHLA-D AntigensHLA-DM antigensantigen presentationautoimmunityhuman leucocyte antigen-DMmajor histocompatibility complex of class IIpeptidomepolymorphism

Identifiers

PMID27534821
PMCPMC5008016
OpenAlexW2507645504

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.