Evidence map›Paper›PMID 28818832›Full record

ArticleAnnals of the rheumatic diseases2017

B cell OX40L supports T follicular helper cell development and contributes to SLE pathogenesis.

Andrea Cortini, Ursula Ellinghaus, Talat H Malik, Deborah S Cunninghame Graham, Marina Botto, Timothy James Vyse

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Regulatory T Cell-Based Adoptive Cell Therapy in Autoimmunity.International journal of molecular sciences · 2025
    Review
  5. Combined TNF-α and OX40L targeting as a new treatment option for hidradenitis suppurativa.The journal of allergy and clinical immunology. Global · 2025
    Article
  6. Review
  7. Review
  8. Human OX40L-CAR-TScience translational medicine · 2024
    Article
  9. Tumour-retained activated CCR7Nature communications · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Immunogenetics of Lupus Erythematosus.Advances in experimental medicine and biology · 2022
    Article
  14. Article
  15. The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022
    Article
  16. Article
  17. Review
  18. Genetic Variants inFrontiers in genetics · 2021
    Article
  19. Article
  20. Observational
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Andrea CortiniDivision of Medical and Molecular Genetics and Immunology, Infection and Inflammatory Disease, King's College London, London, UK.
Ursula EllinghausDivision of Medical and Molecular Genetics and Immunology, Infection and Inflammatory Disease, King's College London, London, UK.
Talat H MalikDepartment of Medicine, Centre for Complement and Inflammation Research, Imperial College London, London, UK.
Deborah S Cunninghame GrahamDivision of Medical and Molecular Genetics and Immunology, Infection and Inflammatory Disease, King's College London, London, UK.
Marina BottoDepartment of Medicine, Centre for Complement and Inflammation Research, Imperial College London, London, UK.
Timothy James VyseDivision of Medical and Molecular Genetics and Immunology, Infection and Inflammatory Disease, King's College London, London, UK.
King's College London · GBCentre for Inflammation Research · GBImperial College London · GB

Funding

Versus Arthritis 20265Versus Arthritis 20332Wellcome Trust
6 · The paper itself

Abstract

objectives

methodsWe used a conditional knockout mouse system to investigate the function of OX40L on B and T lymphocytes in systemic autoimmunity.

resultsPhysiologically, OX40L on both B and T cells contributed to the humoral immune response, but B cell OX40L supported the secondary humoral response and antibody affinity maturation. Our data also indicated that loss of B cell OX40L impeded the generation of splenic T follicular helper cells. We further show that in two models of SLE-a spontaneous congenic model and the H2-IA

conclusionsThese findings contribute to a model in which genetically determined increased OX40L expression promotes human SLE by several mechanisms, contingent on its cellular expression. The improvement in pathology in two models of systemic autoimmunity indicates that OX40L is an excellent therapeutic target in SLE.

Indexed as

AnimalsAutoantibodiesAutoimmunityB-LymphocytesLupus Erythematosus, SystemicMembrane GlycoproteinsMiceMice, KnockoutOX40 LigandT-Lymphocytes, Helper-InducerTumor Necrosis FactorsAutoantibodiesMembrane GlycoproteinsOX40 LigandTnfsf4 protein, mouseTumor Necrosis FactorsautoantibodiesB cellsOX40Lsystemic lupus erythematosusT follicular helper cells

Identifiers

PMID28818832
PMCPMC5705841
OpenAlexW2750202777

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.