Evidence map›Paper›PMID 31562657›Full record

ReviewImmunological reviews2019

BAFF inhibition in SLE-Is tolerance restored?

Shaun W Jackson, Anne Davidson

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

49 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Anti-CD19-engineered exosomes enable B cell-targeted anti-BAFF mRNA delivery to alleviate lupus progression.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. CD4Vaccines · 2025
    Article
  13. Review
  14. Cellular therapies in rheumatic and musculoskeletal diseases.Journal of translational autoimmunity · 2025
    Review
  15. Protective Effects ofBiomedicines · 2025
    Article
  16. Article
  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

2 authors at 2 institutions in 1 country.

Shaun W JacksonSeattle Children's Research Institute, Seattle, WA, USA.
Anne DavidsonFeinstein Institutes for Medical Research, Manhasset, NY, USA.ORCID 0000-0002-4081-6464
Feinstein Institute for Medical Research · USUniversity of Washington · US

Funding

Mechanisms of therapeutic efficacy of BAFF inhibition using belimumabR01AR064811 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DAVIDSON, ANNE · 2014 to 2018
$2.2M
B cell-intrinsic cytokine regulation and B cell-targeted therapies in murine lupuK08AI112993 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI JACKSON, SHAUN WILLIAM · 2014 to 2018
$910k
Belimumab for Maintenance Therapy in Idiopathic Inflammatory MyositisR21AR070540 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DAVIDSON, ANNE · 2017 to 2018
$399k
Novel models for defining function of the BAFF/APRIL cytokine familyR03AI109324 · NIAID · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DAVIDSON, ANNE · 2014 to 2015
$169k
NIAID NIH HHS K08 AI112993NIAID NIH HHS R03 AI109324NIAMS NIH HHS R01 AR064811NIAMS NIH HHS R21 AR070540
6 · The paper itself

Abstract

The B cell activating factor (BAFF) inhibitor, belimumab, is the first biologic drug approved for the treatment of SLE, and exhibits modest, but durable, efficacy in decreasing disease flares and organ damage. BAFF and its homolog APRIL are TNF-like cytokines that support the survival and differentiation of B cells at distinct developmental stages. BAFF is a crucial survival factor for transitional and mature B cells that acts as rheostat for the maturation of low-affinity autoreactive cells. In addition, BAFF augments innate B cell responses via complex interactions with the B cell receptor (BCR) and Toll like receptor (TLR) pathways. In this manner, BAFF impacts autoreactive B cell activation via extrafollicular pathways and fine tunes affinity selection within germinal centers (GC). Finally, BAFF and APRIL support plasma cell survival, with differential impacts on IgM- and IgG-producing populations. Therapeutically, BAFF and combined BAFF/APRIL inhibition delays disease onset in diverse murine lupus strains, although responsiveness to BAFF inhibition is model dependent, in keeping with heterogeneity in clinical responses to belimumab treatment in humans. In this review, we discuss the mechanisms whereby BAFF/APRIL signals promote autoreactive B cell activation, discuss whether altered selection accounts for therapeutic benefits of BAFF inhibition, and address whether new insights into BAFF/APRIL family complexity can be exploited to improve human lupus treatments.

Indexed as

AnimalsAntibodies, Monoclonal, HumanizedB-Cell Activating FactorHumansImmune ToleranceImmunosuppressive AgentsLupus Erythematosus, SystemicReceptors, Antigen, B-CellSignal TransductionTumor Necrosis Factor Ligand Superfamily Member 13Antibodies, Monoclonal, HumanizedB-Cell Activating FactorbelimumabImmunosuppressive AgentsReceptors, Antigen, B-CellTumor Necrosis Factor Ligand Superfamily Member 13BAFFB cellsselectionSLEtolerance

Identifiers

PMID31562657
PMCPMC6935406
OpenAlexW2975257070

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.