Evidence map›Paper›PMID 33519824›Full record

ReviewFrontiers in immunology2020

Recent Advances in Lupus B Cell Biology: PI3K, IFNγ, and Chromatin.

Maria A Bacalao, Anne B Satterthwaite

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  15. Two cases of successful sirolimus treatment for patients with activated phosphoinositide 3-kinase δ syndrome 1.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023
    Article
  16. The Role of B Cell and T Cell Glycosylation in Systemic Lupus Erythematosus.International journal of molecular sciences · 2023
    Review
  17. Article
  18. Article
  19. Review
  20. miR-338-3p blocks TGFβ-induced myofibroblast differentiation through the induction of PTEN.American journal of physiology. Lung cellular and molecular physiology · 2022
    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 1 institution in 1 country.

Maria A BacalaoDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States.
Anne B SatterthwaiteDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States.
The University of Texas Southwestern Medical Center · US

Funding

Regulation and Consequences of Ets1 Downregulation in B CellsR01AI122720 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI GARRETT-SINHA, LEE ANN, SATTERTHWAITE, ANNE B · 2016 to 2020
$2.6M
Tracking Marginal Zone B Cells and Their Progeny in AutoimmunityR21AI137746 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI SATTERTHWAITE, ANNE B · 2018 to 2019
$446k
NIAID NIH HHS R01 AI122720NIAID NIH HHS R21 AI137746
6 · The paper itself

Abstract

In the autoimmune disease Systemic Lupus Erythematosus (SLE), autoantibodies are formed that promote inflammation and tissue damage. There has been significant interest in understanding the B cell derangements involved in SLE pathogenesis. The past few years have been particularly fruitful in three domains: the role of PI3K signaling in loss of B cell tolerance, the role of IFNγ signaling in the development of autoimmunity, and the characterization of changes in chromatin accessibility in SLE B cells. The PI3K pathway coordinates various downstream signaling molecules involved in B cell development and activation. It is governed by the phosphatases PTEN and SHIP-1. Murine models lacking either of these phosphatases in B cells develop autoimmune disease and exhibit defects in B cell tolerance. Limited studies of human SLE B cells demonstrate reduced expression of PTEN or increased signaling events downstream of PI3K in some patients. IFNγ has long been known to be elevated in both SLE patients and mouse models of lupus. New data suggests that IFNγR expression on B cells is required to develop autoreactive germinal centers (GC) and autoantibodies in murine lupus. Furthermore, IFNγ promotes increased transcription of BCL6, IL-6 and T-bet in B cells, which also promote GC and autoantibody formation. IFNγ also induces epigenetic changes in human B cells. SLE B cells demonstrate significant epigenetic reprogramming, including enhanced chromatin accessibility at transcription factor motifs involved in B cell activation and plasma cell (PC) differentiation as well as alterations in DNA methylation and histone modifications. Histone deacetylase inhibitors limit disease development in murine lupus models, at least in part

Indexed as

AnimalsAntibodies, MonoclonalAutoantibodiesAutoimmunityB-LymphocytesChromatinDisease Models, AnimalDNA MethylationGerminal CenterHistone CodeHistone DeacetylasesHumansImmunoglobulin Class SwitchingInterferon-gammaInterferon gamma ReceptorLupus Erythematosus, SystemicAntibodies, MonoclonalAutoantibodiesChromatinHistone DeacetylasesInterferon-gammaInterferon gamma ReceptorPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesReceptors, InterferonautoimmunityB cellchromatinIFNγlupusPI3Ktolerance

Identifiers

PMID33519824
PMCPMC7841329
OpenAlexW3119966503

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.