Evidence map›Paper›PMID 31631359›Full record

ReviewImmunological reviews2019

Autoreactive B cells in SLE, villains or innocent bystanders?

Jennie A Hamilton, Hui-Chen Hsu, John D Mountz

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 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.1field-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

45 citing papers in PubMed, 76 citations in OpenAlex.

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  8. The role of fatty acid metabolism on B cells and B cell-related autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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 1 institution in 1 country.

Jennie A HamiltonUniversity of Alabama at Birmingham, Birmingham, AL, USA.
Hui-Chen HsuUniversity of Alabama at Birmingham, Birmingham, AL, USA.
John D MountzUniversity of Alabama at Birmingham, Birmingham, AL, USA.ORCID 0000-0001-9061-3158
University of Alabama at Birmingham · US

Funding

Virology CoreP30AI027767 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI OLAF KUTSCH · 1988 to 2026
$84.1M
IMMUNOLOGIC DISEASES AND BASIC IMMUNOLOGYT32AI007051 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Laurie Ellen Harrington · 1985 to 2026
$13.1M
ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
Suppression of pathogenic autoantibodies in lupus by inhibition of AIDR01AI071110 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2008 to 2018
$4.0M
B cell intrinsic interferon-beta regulates autoreactive B cell developmentR01AI134023 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2018 to 2022
$2.4M
Entry of antigen-presenting B cells into the follicle directed by IFNa and IL-17R01AI083705 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HSU, HUI-CHEN · 2011 to 2015
$1.8M
Regulation of Migration of Autoreactive Germinal Centers and Precursor B CellsI01BX000600 · VA · BIRMINGHAM VA MEDICAL CENTER · PI MOUNTZ, JOHN D · 2009 to 2017
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Interferon Beta Initiated Development of Immunogenic T1 B cells in LupusI01BX004049 · VA · BIRMINGHAM VA MEDICAL CENTER · PI MOUNTZ, JOHN D · 2018 to 2022
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BLRD VA I01 BX000600BLRD VA I01 BX004049NIAID NIH HHS P30 AI027767NIAID NIH HHS R01 AI071110NIAID NIH HHS R01 AI083705NIAID NIH HHS R01 AI134023NIAID NIH HHS T32 AI007051NIAMS NIH HHS P30 AR048311
6 · The paper itself

Abstract

The current concepts for development of autoreactive B cells in SLE (systemic lupus erythematosus) focus on extrinsic stimuli and factors that provoke B cells into tolerance loss. Traditionally, major tolerance loss pathways are thought to be regulated by factors outside the B cell including autoantigen engagement of the B-cell receptor (BCR) with simultaneous type I interferon (IFN) produced by dendritic cells, especially plasmacytoid dendritic cells (pDCs). Later, in autoreactive follicles, B-cells encounter T-follicular helper cells (Tfh) that produce interleukin (IL)-21, IL-4 and pathogenic cytokines, IL-17 and IFN gamma (IFNɣ). This review discusses these mechanisms and also highlights recent advances pointing to the peripheral transitional B-cell stage as a major juncture where transient autocrine IFNβ expression by developing B-cells imprints a heightened susceptibility to external factors favoring differentiation into autoantibody-producing plasmablasts. Recent studies highlight transitional B-cell heterogeneity as a determinant of intrinsic resistance or susceptibility to tolerance loss through the shaping of B-cell responsiveness to cytokines and other environment factors.

Indexed as

AnimalsAutoantibodiesAutoimmunityB-LymphocytesCytokinesDendritic CellsHumansImmune ToleranceLupus Erythematosus, SystemicT-Lymphocytes, Helper-InducerAutoantibodiesCytokinesautoantibodiesautoimmunityBXD2follicular T-helper cellsgerminal center B cellsIFNβIL-17IL-21lupuslymphotoxin betamarginal zone macrophagesmarginal zone-precursor B cellsplasmacytoid dendritic cellsregulator of G-protein signalingSLEtransitional stage 1 B cellstype I IFNs

Identifiers

PMID31631359
PMCPMC6935412
OpenAlexW2981813202

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.