Evidence map›Paper›PMID 33658999›Full record

ArticleFrontiers in immunology2020

CD52 Is Elevated on B cells of SLE Patients and Regulates B Cell Function.

Kartik Bhamidipati, John L Silberstein, Yashaar Chaichian, Matthew C Baker, Tobias V Lanz, Amin Zia, Yusuf S Rasheed, Jennifer R Cochran, William H Robinson

Open access · goldAbstract read
In one paragraph

Article 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, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  14. Fine-mapping causal tissues and genes at disease-associated loci.medRxiv : the preprint server for health sciences · 2024
    Article
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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

9 authors at 2 institutions in 2 countries.

Kartik BhamidipatiProgram in Immunology, Stanford University School of Medicine, Stanford, CA, United States.
John L SilbersteinProgram in Immunology, Stanford University School of Medicine, Stanford, CA, United States.
Yashaar ChaichianDivision of Immunology and Rheumatology, School of Medicine, Stanford University, Stanford, CA, United States.
Matthew C BakerDivision of Immunology and Rheumatology, School of Medicine, Stanford University, Stanford, CA, United States.
Tobias V LanzVA Palo Alto Healthcare System, Palo Alto, CA, United States.
Amin ZiaVA Palo Alto Healthcare System, Palo Alto, CA, United States.
Yusuf S RasheedDepartment of Bioengineering, Stanford University, Stanford, CA, United States.
Jennifer R CochranDepartment of Bioengineering, Stanford University, Stanford, CA, United States.
William H RobinsonVA Palo Alto Healthcare System, Palo Alto, CA, United States.
Stanford University · USVA Palo Alto Health Care System · US

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Prevention Center U01: Early Targets for Antigen-Specific Tolerance Induction in Preclinical Rheumatoid ArthritisU01AI101981 · NIAID · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 2012 to 2021
$6.2M
Evolving Adaptive and Effector Mechanisms from Pre-RA Through Established DiseaseUH2AR067681 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 2014 to 2020
$5.5M
Large-Scale Characterization of Autoantibody Responses in Rheumatoid ArthritisR01AR063676 · NIAMS · STANFORD UNIVERSITY · PI ROBINSON, WILLIAM H · 2013 to 2017
$1.7M
NIAID NIH HHS T32 AI007290NIAID NIH HHS U01 AI101981NIAMS NIH HHS R01 AR063676NIAMS NIH HHS UH2 AR067681
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by B cell dysregulation and breaks in tolerance that lead to the production of pathogenic autoantibodies. We performed single-cell RNA sequencing of B cells from healthy donors and individuals with SLE which revealed upregulated CD52 expression in SLE patients. We further demonstrate that SLE patients exhibit significantly increased levels of B cell surface CD52 expression and plasma soluble CD52, and levels of soluble CD52 positively correlate with measures of lupus disease activity. Using CD52-deficient JeKo-1 cells, we show that cells lacking surface CD52 expression are hyperresponsive to B cell receptor (BCR) signaling, suggesting an inhibitory role for the surface-bound protein. In healthy donor B cells, antigen-specific BCR-activation initiated CD52 cleavage in a phospholipase C dependent manner, significantly reducing cell surface levels. Experiments with recombinant CD52-Fc showed that soluble CD52 inhibits BCR signaling in a manner partially-dependent on Siglec-10. Moreover, incubation of unstimulated B cells with CD52-Fc resulted in the reduction of surface immunoglobulin and CXCR5. Prolonged incubation of B cells with CD52 resulted in the expansion of IgD+IgM

Indexed as

AutoantibodiesB-LymphocytesCD52 AntigenChemokine CXCL13Gene Expression RegulationGenes, MHC Class IIHumansImmunoglobulin GImmunoglobulin MLupus Erythematosus, SystemicReceptors, Antigen, B-CellReceptors, CXCR5RNA-SeqSeverity of Illness IndexSignal TransductionSingle-Cell AnalysisAutoantibodiesCD52 AntigenCD52 protein, humanChemokine CXCL13CXCL13 protein, humanCXCR5 protein, humanImmunoglobulin GImmunoglobulin MReceptors, Antigen, B-CellReceptors, CXCR5Type C PhospholipasesautoimmunityB cell receptor signalingB cellsglycoproteinsystemic lupus erythematosus

Identifiers

PMID33658999
PMCPMC7917337
OpenAlexW3128917639

What OpenQuestion holds

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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 OpenQuestion graph.