Evidence map›Paper›PMID 27655102›Full record

ReviewDigestive diseases and sciences2016

B Cell-Activating Factor (BAFF)-Targeted B Cell Therapies in Inflammatory Bowel Diseases.

Mathieu Uzzan, Jean-Frederic Colombel, Andrea Cerutti, Xavier Treton, Saurabh Mehandru

Abstract readReview
PubMed Publisher
In one paragraph

Review in Digestive diseases and sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Protective Effects ofBiomedicines · 2025
    Article
  6. Review
  7. Forging the Future: B Cell Activating Factor's Impact on Nephrotic Syndrome.The Malaysian journal of medical sciences : MJMS · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. IgA nephropathy associated with Crohn's disease.World journal of methodology · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  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

5 authors at 2 institutions in 2 countries.

Mathieu UzzanDivision of Gastroenterology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. mathieuuzzan@gmail.com.ORCID 0000-0002-7761-2879
Jean-Frederic ColombelDivision of Gastroenterology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Andrea CeruttiThe Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Xavier TretonDepartment of Gastroenterology, Beaujon Hospital, APHP, Denis Diderot University, Paris, France.
Saurabh MehandruDivision of Gastroenterology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Icahn School of Medicine at Mount Sinai · USUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel diseases (IBD) involve dysregulated immune responses to gut antigens in genetically predisposed individuals. While a better elucidation of IBD pathophysiology has considerably increased the number of treatment options, the need for more effective therapeutic strategies remains a pressing priority. Defects of both non-hematopoietic (epithelial and stromal) and hematopoietic (lymphoid and myeloid) cells have been described in patients with IBD. Within the lymphoid system, alterations of the T cell compartment are viewed as essential in the pathogenesis of IBD. However, growing evidence points to the additional perturbations of the B cell compartment. Indeed, the intestinal lamina propria from IBD patients shows an increased presence of antibody-secreting plasma cells, which correlates with enhanced pro-inflammatory immunoglobulin G production and changes in the quality of non-inflammatory IgA responses. These B cell abnormalities are compounded by the emergence of systemic antibody responses to various autologous and microbial antigens, which predates the clinical diagnosis of IBD and identifies patients with complicated disease. It is presently unclear whether such antibody responses play a pathogenetic role, as B cell depletion with the CD20-targeting monoclonal antibody rituximab did not ameliorate ulcerative colitis in a clinical trial. However, it must be noted that unresponsiveness to rituximab is also observed also in some patients with autoimmune disorders usually responsive to B cell-depleting therapies. In this review, we discussed mechanistic aspects of B cell-based therapies and their potential role in IBD with a special interest on BAFF and BAFF-targeting therapies buoyed by the success of anti-BAFF treatments in rheumatologic disorders.

Indexed as

Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedB-Cell Activating FactorB-Cell Activation Factor ReceptorB-Cell Maturation AntigenB-LymphocytesDendritic CellsHumansImmunity, HumoralImmunoglobulin Class SwitchingImmunoglobulin GImmunologic FactorsImmunosuppressive AgentsInflammatory Bowel DiseasesMolecular Targeted TherapyMonocytesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedB-Cell Activating FactorB-Cell Activation Factor ReceptorB-Cell Maturation AntigenbelimumabImmunoglobulin GImmunologic FactorsImmunosuppressive AgentsRecombinant Fusion ProteinsRituximabtabalumabTACI receptor-IgG Fc fragment fusion proteinTransmembrane Activator and CAML Interactor ProteinBAFFB cellsInflammatory bowel diseases

Identifiers

PMID27655102
OpenAlexW2521063508

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.