Evidence map›Paper›PMID 30854633›Full record

ArticleEuropean journal of immunology2019

CD1b presents self and Borrelia burgdorferi diacylglycerols to human T cells.

Peter Reinink, Michael N T Souter, Tan-Yun Cheng, Tamara van Gorkom, Stefanie Lenz, Joanna Kubler-Kielb, Klemen Strle, Kristin Kremer, Steven F T Thijsen, Allen C Steere and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Cell-Mediated Cytotoxicity in Lyme Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. Immune Response toCurrent issues in molecular biology · 2021
    Article
  10. Review
  11. 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

14 authors at 7 institutions in 6 countries.

Peter ReininkDepartment of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.
Michael N T SouterDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
Tan-Yun ChengBrigham and Women's Hospital Division of Rheumatology, Immunology and Allergy, Harvard Medical School, Boston, MA, USA.
Tamara van GorkomDepartment of Medical Microbiology and Immunology, Diakonessen Hospital, Utrecht, The Netherlands.
Stefanie LenzDepartment of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.
Joanna Kubler-KielbNational Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Klemen StrleCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Kristin KremerCentre for Infectious Diseases Research, Diagnostics and Laboratory Surveillance, Centre for Infectious Diseases Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
Steven F T ThijsenDepartment of Medical Microbiology and Immunology, Diakonessen Hospital, Utrecht, The Netherlands.
Allen C SteereCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Dale I GodfreyDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
Daniel G PellicciDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
D Branch MoodyBrigham and Women's Hospital Division of Rheumatology, Immunology and Allergy, Harvard Medical School, Boston, MA, USA.
Ildiko Van RhijnDepartment of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0002-1446-5701
Brigham and Women's Hospital · USThe University of Melbourne · AUHarvard University · USNational Institute for Public Health and the Environment · NLDiakonessenhuis hospital · NLNational Institutes of Health · USUtrecht University · NL

Funding

T cell response to CDI-restricted lipids in tuberculosisR01AI049313 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI MOODY, DAVID BRANCH · 2001 to 2025
$10.6M
Borrelia burgdorferi-Induced Autoimmunity in Lyme DiseaseR01AI101175 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI STEERE, ALLEN C · 2013 to 2021
$3.6M
Cellular and humoral immunity in Lyme arthritisR01AI144365 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI STEERE, ALLEN C · 2019 to 2023
$2.9M
Role of Tuberculosinyl Metabolites in M. Tuberculosis VirulenceR01AI116604 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI MOODY, DAVID BRANCH · 2015 to 2019
$2.4M
NIAID NIH HHS R01 AI049313NIAID NIH HHS R01 AI101175NIAID NIH HHS R01 AI116604NIAID NIH HHS R01 AI144365
6 · The paper itself

Abstract

Lyme disease is a common multisystem disease caused by infection with a tick-transmitted spirochete, Borrelia burgdorferi and related Borrelia species. The monoglycosylated diacylglycerol known as B. burgdorferi glycolipid II (BbGL-II) is a major target of antibodies in sera from infected individuals. Here, we show that CD1b presents BbGL-II to human T cells and that the TCR mediates the recognition. However, we did not detect increased frequency of CD1b-BbGL-II binding T cells in the peripheral blood of Lyme disease patients compared to controls. Unexpectedly, mapping the T cell specificity for BbGL-II-like molecules using tetramers and activation assays revealed a concomitant response to CD1b-expressing APCs in absence of BbGL-II. Further, among all major classes of self-lipid tested, BbGL-II responsive TCRs show strong cross-reactivity to diacylglycerol, a self-lipid antigen with structural similarities to BbGL-II. Extending prior work on MHC and CD1b, CD1c, and CD1d proteins, this study provides evidence for cross-reactive CD1b-restricted T cell responses to bacterial and self-antigens, and identifies chemically defined targets for future discovery of self and foreign antigen cross-reactive T cells.

Indexed as

Antigen PresentationAntigens, BacterialAntigens, CD1AutoantigensBorrelia burgdorferiCross ReactionsDiglyceridesEpitopes, T-LymphocyteHumansLyme DiseaseLymphocyte ActivationProtein BindingReceptors, Antigen, T-CellT-Lymphocytes1,2-diacylglycerolAntigens, BacterialAntigens, CD1AutoantigensCD1b antigenDiglyceridesEpitopes, T-LymphocyteReceptors, Antigen, T-Cellantigen specificityCD1blipid antigenLyme diseaseT cells

Identifiers

PMID30854633
PMCPMC6594241
OpenAlexW2920875243

What OpenQuestion holds

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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.