Evidence map›Paper›PMID 30849450›Full record

ReviewHuman immunology2019

B cells in chronic graft-versus-host disease.

William McManigle, Ayman Youssef, Stefanie Sarantopoulos

Open access · greenAbstract readReview
In one paragraph

Review in Human immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
7.2field-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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Observational
  8. Review
  9. Review
  10. Article
  11. Therapeutic efficacy of rituximab combined with cyclosporin A on B-cell dysregulation in chronic graft-versus-host disease.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  12. Article
  13. Review
  14. Review
  15. Graft-Versus-Host Disease Mouse Models: A Clinical-Translational Perspective.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  16. Review
  17. Review
  18. Review
  19. 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 2 countries.

William McManigleDivision of Pulmonary, Allergy, and Critical Care Medicine, Duke University, Durham, NC, USA; Department of Medicine, Duke University, Durham, NC, USA.
Ayman YoussefAdult Hematology and Bone Marrow Transplantation, Alexandria Faculty of Medicine, Alexandria, Egypt.
Stefanie SarantopoulosDepartment of Medicine, Duke University, Durham, NC, USA; Division of Hematologic Malignancies and Cellular Therapy, Duke University, Durham, NC, USA; Duke Cancer Institute, Duke University, Durham, NC, USA. Electronic address: stefanie.sarantopoulos@duke.edu.
Duke University · USAlexandria University · EG

Funding

Pathological B Cells: Novel Strategies to Prevent and Treat Chronic GVHDR01HL129061 · NHLBI · DUKE UNIVERSITY · PI Stefanie Sarantopoulos · 2015 to 2026
$7.7M
NHLBI NIH HHS R01 HL129061
6 · The paper itself

Abstract

Allogeneic hematopoietic stem cell transplantation (alloHCT) is the definitive therapy for numerous otherwise incurable hematologic malignancies and non-malignant diseases. The genetic disparity between donor and recipient both underpins therapeutic effects and confers donor immune system-mediated damage in the recipient, called graft-versus-host disease (GVHD). Chronic GVHD (cGVHD) is a major cause of late post-transplant morbidity and mortality. B cells have a substantiated role in cGVHD pathogenesis, as first demonstrated by clinical response to the anti-CD20 monoclonal antibody, rituximab. Initiation of CD20 blockade is met at times with limited therapeutic success that has been associated with altered peripheral B cell homeostasis and excess B Cell Activating Factor of the TNF family (BAFF). Increased BAFF to B cell ratios are associated with the presence of circulating, constitutively activated B cells in patients with cGVHD. These cGVHD patient B cells have increased survival capacity and signal through both BAFF-associated and B Cell Receptor (BCR) signaling pathways. Proximal BCR signaling molecules, Syk and BTK, appear to be hyper-activated in cGVHD B cells and can be targeted with small molecule inhibitors. Murine studies have confirmed roles for Syk and BTK in development of cGVHD. Emerging evidence has prompted investigation of several small molecule inhibitors in an attempt to restore B cell homeostasis and potentially target rare, pathologic B cell populations.

Indexed as

Hematopoietic Stem Cell TransplantationAgammaglobulinaemia Tyrosine KinaseAnimalsB-Cell Activating FactorB-LymphocytesChronic DiseaseGraft vs Host DiseaseHomeostasisHumansImmunotherapyMiceReceptors, Antigen, B-CellRituximabSignal TransductionSyk KinaseAgammaglobulinaemia Tyrosine KinaseB-Cell Activating FactorBTK protein, humanReceptors, Antigen, B-CellRituximabSyk KinaseTNFSF13B protein, humanAllogeneic hematopoietic stem cell transplantation (AlloHCT)Autologous hematopoietic stem cell transplantation (autoHCT)B cell activation factor (BAFF)B cell linker (Blnk) proteinB cell receptor (BCR)B cellsChronic graft-versus-host disease (cGVHD)Graft-versus-host disease (GVHD)Spleen tyrosine kinase (Syk) protein

Identifiers

PMID30849450
PMCPMC8049519
OpenAlexW2920344309

What OpenQuestion holds

Textmetadata
LicenceTDM
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.