Evidence map›Paper›PMID 36182705›Full record

ArticleCellular immunology2022

BAFF antagonism via the BAFF receptor 3 binding site attenuates BAFF 60-mer-induced classical NF-κB signaling and metabolic reprogramming of B cells.

Melissa D Lempicki, Saikat Paul, Vlad Serbulea, Clint M Upchurch, Srabani Sahu, Jake A Gray, Gorav Ailawadi, Brandon L Garcia, Coleen A McNamara, Norbert Leitinger and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

11 authors at 2 institutions in 1 country.

Melissa D LempickiDepartment of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27858, United States.
Saikat PaulDepartment of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27858, United States.
Vlad SerbuleaDepartment of Pharmacology, University of Virginia, VA 22908, United States.
Clint M UpchurchDepartment of Pharmacology, University of Virginia, VA 22908, United States.
Srabani SahuDepartment of Pharmacology, University of Virginia, VA 22908, United States.
Jake A GrayDepartment of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27858, United States.
Gorav AilawadiDepartment of Surgery, University of Virginia, VA 22908, United States.
Brandon L GarciaDepartment of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27858, United States.
Coleen A McNamaraRobert M. Berne Cardiovascular Research Center, University of Virginia, VA 22908, United States.
Norbert LeitingerDepartment of Pharmacology, University of Virginia, VA 22908, United States.
Akshaya K MeherDepartment of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27858, United States; Department of Pharmacology, University of Virginia, VA 22908, United States. Electronic address: mehera19@ecu.edu.
University of Virginia · USEast Carolina University · US

Funding

BAFF 60mer as a novel therapeutic target for vascular diseasesR01HL146685 · NHLBI · UNIVERSITY OF VIRGINIA · PI MEHER, AKSHAYA KUMAR · 2019 to 2022
$1.5M
Role of Dab2 in Fatty Liver DiseaseR01DK096076 · NIDDK · UNIVERSITY OF VIRGINIA · PI LEITINGER, NORBERT · 2013 to 2016
$1.4M
NHLBI NIH HHS R01 HL146685NIDDK NIH HHS R01 DK096076
6 · The paper itself

Abstract

Human recombinant B cell activating factor (BAFF) is secreted as 3-mers, which can associate to form 60-mers in culture supernatants. However, the presence of BAFF multimers in humans is still debated and it is incompletely understood how BAFF multimers activate the B cells. Here, we demonstrate that BAFF can exist as 60-mers or higher order multimers in human plasma. In vitro, BAFF 60-mer strongly induced the transcriptome of B cells which was partly attenuated by antagonism using a soluble fragment of BAFF receptor 3. Furthermore, compared to BAFF 3-mer, BAFF 60-mer strongly induced a transient classical and prolonged alternate NF-κB signaling, glucose oxidation by both aerobic glycolysis and oxidative phosphorylation, and succinate utilization by mitochondria. BAFF antagonism selectively attenuated classical NF-κB signaling and glucose oxidation. Altogether, our results suggest critical roles of BAFF 60-mer and its BAFF receptor 3 binding site in hyperactivation of B cells.

Indexed as

B-Cell Activating FactorNF-kappa BB-Cell Activation Factor ReceptorBinding SitesGlucoseHumansMetabolic ReprogrammingB-Cell Activating FactorB-Cell Activation Factor ReceptorGlucoseNF-kappa BBAFF multimersB cell activationMetabolic reprogrammingNF-κB signalingTranscriptomics

Identifiers

PMID36182705
PMCPMC10691782
OpenAlexW4295138688

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.