Evidence map›Paper›PMID 29997289›Full record

ArticleJCI insight2018

Defective BTLA functionality is rescued by restoring lipid metabolism in lupus CD4+ T cells.

Matthieu Sawaf, Jean-Daniel Fauny, Renaud Felten, Flora Sagez, Jacques-Eric Gottenberg, Hélène Dumortier, Fanny Monneaux

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. CD4Precision clinical medicine · 2022
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. T cell Metabolism in Lupus.Immunometabolism · 2020
    Article
  18. Article
  19. Immune cell metabolism in autoimmunity.Clinical and experimental immunology · 2019
    Review
  20. 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

7 authors at 1 institution in 1 country.

Matthieu SawafCNRS, Institut de Biologie Moléculaire et Cellulaire, Immunologie, Immunopathologie et Chimie Thérapeutique, Strasbourg, France.
Jean-Daniel FaunyCNRS, Institut de Biologie Moléculaire et Cellulaire, Immunologie, Immunopathologie et Chimie Thérapeutique, Strasbourg, France.
Renaud FeltenCNRS, Institut de Biologie Moléculaire et Cellulaire, Immunologie, Immunopathologie et Chimie Thérapeutique, Strasbourg, France.
Flora SagezCNRS, Institut de Biologie Moléculaire et Cellulaire, Immunologie, Immunopathologie et Chimie Thérapeutique, Strasbourg, France.
Jacques-Eric GottenbergCNRS, Institut de Biologie Moléculaire et Cellulaire, Immunologie, Immunopathologie et Chimie Thérapeutique, Strasbourg, France.
Hélène DumortierCNRS, Institut de Biologie Moléculaire et Cellulaire, Immunologie, Immunopathologie et Chimie Thérapeutique, Strasbourg, France.
Fanny MonneauxCNRS, Institut de Biologie Moléculaire et Cellulaire, Immunologie, Immunopathologie et Chimie Thérapeutique, Strasbourg, France.
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coinhibitory receptors play an important role in the prevention of autoimmune diseases, such as systemic lupus erythematosus (SLE), by limiting T cell activation. B and T lymphocyte attenuator (BTLA) is an inhibitory receptor, similar to cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and programmed death 1 (PD1), that negatively regulates the immune response. The role of BTLA in the pathogenesis of autoimmune diseases in humans and, more specifically, in SLE is largely unknown. We investigated BTLA expression on various T cell subsets, and we did not observe significant variations of BTLA expression between lupus patients and healthy controls. However, the enhancement of BTLA expression after activation was significantly lower in SLE patients compared with that in healthy controls. Furthermore, we found an impaired capacity of BTLA to inhibit T cell activation in SLE due to a poor BTLA recruitment to the immunological synapse following T cell stimulation. Finally, we demonstrated that defective BTLA function can be corrected by restoring intracellular trafficking and by normalizing the lipid metabolism in lupus CD4+ T cells. Collectively, our results evidence that the BTLA signaling pathway is altered in SLE T cells and highlight the potential of targeting this pathway for the development of new therapeutic strategies in lupus.

Indexed as

Lipid MetabolismAdolescentAdultAgedAged, 80 and overAutoimmune DiseasesCD4-Positive T-LymphocytesCell ProliferationCTLA-4 AntigenFemaleFranceHumansLupus Erythematosus, SystemicLymphocyte ActivationMaleMiddle AgedBTLA protein, humanCTLA-4 AntigenCTLA4 protein, humanPDCD1 protein, humanProgrammed Cell Death 1 ReceptorReceptors, ImmunologicAutoimmunityImmunologyLupus

Identifiers

PMID29997289
PMCPMC6124536
OpenAlexW2823373950

What OpenQuestion holds

Textmetadata
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.