Evidence map›Paper›PMID 38642912›Full record

ReviewClinical and experimental immunology2024

Disrupting B and T-cell collaboration in autoimmune disease: T-cell engagers versus CAR T-cell therapy?

Kavina Shah, Maria Leandro, Mark Cragg, Florian Kollert, Franz Schuler, Christian Klein, Venkat Reddy

Open access · hybridAbstract readReview
In one paragraph

Review in Clinical and experimental immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Potential new targets for rheumatic diseases.EULAR rheumatology open · 2026
    Review
  7. Review
  8. Review
  9. Can we cure autoimmunity?Current opinion in immunology · 2026
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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 4 institutions in 2 countries.

Kavina ShahCentre for Rheumatology, UCLH, London,UK.
Maria LeandroCentre for Rheumatology, UCLH, London,UK.
Mark CraggUniversity of Southampton Faculty of Medicine, Antibody and Vaccine Group, Centre for Cancer Immunology, University of Southampton, Southampton, UK.
Florian KollertRoche Innovation Center Basel, Early Development Immunology, Infectious Diseases & Ophthalmology, Basel, Switzerland.
Franz SchulerRoche Innovation Center Basel, Roche Pharma Research and Early Development, Schlieren, Switzerland.
Christian KleinRoche Innovation Center Zurich, Cancer Immunotherapy Discovery, Oncology Discovery & Translational Area, Schlieren, Switzerland.
Venkat ReddyCentre for Rheumatology, UCLH, London,UK.ORCID 0000-0002-3757-4425
Roche (Switzerland) · CHUniversity College Hospital · GBBritish Society for Rheumatology · GBUniversity of Southampton · GB

Funding

Cancer Research UK DRCRPG-MAY23/100001Medical Research Council MR/T024968/1
6 · The paper itself

Abstract

B and T cells collaborate to drive autoimmune disease (AID). Historically, B- and T-cell (B-T cell) co-interaction was targeted through different pathways such as alemtuzumab, abatacept, and dapirolizumab with variable impact on B-cell depletion (BCD), whereas the majority of patients with AID including rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and organ transplantation benefit from targeted BCD with anti-CD20 monoclonal antibodies such as rituximab, ocrelizumab, or ofatumumab. Refractory AID is a significant problem for patients with incomplete BCD with a greater frequency of IgD-CD27+ switched memory B cells, CD19+CD20- B cells, and plasma cells that are not directly targeted by anti-CD20 antibodies, whereas most lymphoid tissue plasma cells express CD19. Furthermore, B-T-cell collaboration is predominant in lymphoid tissues and at sites of inflammation such as the joint and kidney, where BCD may be inefficient, due to limited access to key effector cells. In the treatment of cancer, chimeric antigen receptor (CAR) T-cell therapy and T-cell engagers (TCE) that recruit T cells to induce B-cell cytotoxicity have delivered promising results for anti-CD19 CAR T-cell therapies, the CD19 TCE blinatumomab and CD20 TCE such as mosunetuzumab, glofitamab, or epcoritamab. Limited evidence suggests that anti-CD19 CAR T-cell therapy may be effective in managing refractory AID whereas we await evaluation of TCE for use in non-oncological indications. Therefore, here, we discuss the potential mechanistic advantages of novel therapies that rely on T cells as effector cells to disrupt B-T-cell collaboration toward overcoming rituximab-resistant AID.

Indexed as

Autoimmune DiseasesB-LymphocytesImmunotherapy, AdoptiveT-LymphocytesAnimalsCell CommunicationHumansReceptors, Chimeric AntigenRituximabReceptors, Chimeric AntigenRituximabCAR T-cell therapyrheumatoid arthritisrituximabsystemic lupus erythematosusT-cell engagers

Identifiers

PMID38642912
PMCPMC11188544
OpenAlexW4394976136

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.