Evidence map›Paper›PMID 31426619›Full record

ReviewCells2019

Targeting the CD40-CD154 Signaling Pathway for Treatment of Autoimmune Arthritis.

Jenn-Haung Lai, Shue-Fen Luo, Ling-Jun Ho

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. 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
2.1field-weighted citation impact, top 12% 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, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Genetics and epigenetics of autoimmune thyroid diseases: Translational implications.Best practice & research. Clinical endocrinology & metabolism · 2023
    Review
  10. FcγRs and Their Relevance for the Activity of Anti-CD40 Antibodies.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Dendritic cell biology and its role in tumor immunotherapy.Journal of hematology & oncology · 2020
    Review
  18. Article
  19. Percentages of CD4+CD8+ Double-positive T Lymphocytes in the Peripheral Blood of Adults from a Blood Bank in Bogotá, ColombiaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2020
    Article
  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

3 authors at 2 institutions in 1 country.

Jenn-Haung LaiDivision of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305, Taiwan. laiandho@gmail.com.ORCID 0000-0002-6266-705X
Shue-Fen LuoDivision of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305, Taiwan.
Ling-Jun HoInstitute of Cellular and System Medicine, National Health Research Institute, Zhunan 35053, Taiwan. lingjunho@nhri.org.tw.ORCID 0000-0003-3453-2913
Chang Gung University · TWNational Health Research Institutes · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Full activation of T lymphocytes requires signals from both T cell receptors and costimulatory molecules. In addition to CD28, several T cell molecules could deliver costimulatory signals, including CD154, which primarily interacts with CD40 on B-cells. CD40 is a critical molecule regulating several B-cell functions, such as antibody production, germinal center formation and cellular proliferation. Upregulated expression of CD40 and CD154 occurs in immune effector cells and non-immune cells in different autoimmune diseases. In addition, therapeutic benefits have been observed by blocking the CD40-CD154 interaction in animals with collagen-induced arthritis. Given the therapeutic success of the biologics abatacept, which blocks CD28 costimulation, and rituximab, which deletes B cells in the treatment of autoimmune arthritis, the inhibition of the CD40-CD154 axis has two advantages, namely, attenuating CD154-mediated T cell costimulation and suppressing CD40-mediated B-cell stimulation. Furthermore, blockade of the CD40-CD154 interaction drives the conversion of CD4+ T cells to regulatory T cells that mediate immunosuppression. Currently, several biological products targeting the CD40-CD154 axis have been developed and are undergoing early phase clinical trials with encouraging success in several autoimmune disorders, including autoimmune arthritis. This review addresses the roles of the CD40-CD154 axis in the pathogenesis of autoimmune arthritis and its potential as a therapeutic target.

Indexed as

ArthritisAutoimmune DiseasesAbataceptAnimalsAntirheumatic AgentsB-LymphocytesCD40 AntigensCD40 LigandCD4-Positive T-LymphocytesCells, CulturedHumansLymphocyte ActivationMiceRituximabSignal TransductionAbataceptAntirheumatic AgentsCD40 AntigensCD40 LigandRituximabarthritisautoimmuneCD154CD40costimulation

Identifiers

PMID31426619
PMCPMC6721639
OpenAlexW2967969561

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.