Evidence map›Paper›PMID 35027402›Full record

ArticleAnnals of the rheumatic diseases2022

Key interactions in the trimolecular complex consisting of the rheumatoid arthritis-associated DRB1*04:01 molecule, the major glycosylated collagen II peptide and the T-cell receptor.

Changrong Ge, Sylvia Weisse, Bingze Xu, Doreen Dobritzsch, Johan Viljanen, Jan Kihlberg, Nhu-Nguyen Do, Nadine Schneider, Harald Lanig, Rikard Holmdahl and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

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  15. Therapy targeting antigen-specific T cells by a peptide-based tolerizing vaccine against autoimmune arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

11 authors at 6 institutions in 3 countries.

Changrong Ge *Section for Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Sylvia Weisse *Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, Frankfurt am Main, Germany.
Bingze XuSection for Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Doreen DobritzschSection of Biochemistry, Department of Chemistry-BMC, Uppsala University, Uppsala, Sweden.
Johan ViljanenSection of Organic Chemistry, Department of Chemistry-BMC, Uppsala University, Uppsala, Sweden.
Jan KihlbergSection of Organic Chemistry, Department of Chemistry-BMC, Uppsala University, Uppsala, Sweden.
Nhu-Nguyen DoSection for Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Nadine SchneiderFraunhofer Institute for Translational Medicine and Pharmacology ITMP, Frankfurt am Main, Germany.
Harald LanigCentral Institute for Scientific Computing (ZISC), Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Rikard HolmdahlSection for Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.ORCID 0000-0002-4969-2576
Harald BurkhardtFraunhofer Institute for Translational Medicine and Pharmacology ITMP, Frankfurt am Main, Germany Harald.Burkhardt@kgu.de.ORCID 0000-0002-6261-3131
Karolinska Institutet · SEUppsala University · SEFraunhofer Institute for Translational Medicine and Pharmacology · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DESecond Affiliated Hospital of Xi'an Jiaotong University · CNUniversity Hospital Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesRheumatoid arthritis (RA) is an autoimmune disease strongly associated with the major histocompatibility complex (MHC) class II allele DRB1*04:01, which encodes a protein that binds self-peptides for presentation to T cells. This study characterises the autoantigen-presenting function of DRB1*04:01 (HLA-DRA*01:01/HLA-DRB1*04:01) at a molecular level for prototypic T-cell determinants, focusing on a post-translationally modified collagen type II (Col2)-derived peptide.

methodsThe crystal structures of DRB1*04:01 molecules in complex with the peptides HSP70

resultsThe crystal structures identified peptide binding to DRB1*04:01 and potential side chain exposure to T cells. The main TCR recognition sites in Col2

conclusionsThe MHC-peptide-TCR interactions elucidated in our study provide new molecular insights into recognition of a post-translationally modified RA T-cell determinant with a known dominant role in arthritogenic and tolerogenic responses in murine Col2-induced arthritis.

Indexed as

Arthritis, RheumatoidLeukocytes, MononuclearAnimalsCollagenHLA-DRB1 ChainsHumansLysineMicePeptidesReceptors, Antigen, T-CellCollagenglycosylated collagenHLA-DRB1 ChainsLysinePeptidesReceptors, Antigen, T-Cellautoimmunityrheumatoid arthritisT-lymphocyte subsets

Identifiers

PMID35027402
PMCPMC8921575
OpenAlexW4205305540

What OpenQuestion holds

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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.