Evidence map›Paper›PMID 35325077›Full record

ArticleRheumatology (Oxford, England)2022

Soluble LILRA3 is aberrantly expressed in antiphospholipid syndrome (APS) and is a potential marker of thrombotic APS.

Hongjiang Liu, Chun Li, Hui Shi, Yixue Guo, Yundi Tang, Chen Chen, Zhen Zhao, Claire K Hoy, Srilakshmi Yalavarthi, Gabriel Figueroa-Parra and 5 more

Abstract read
In one paragraph

Article in Rheumatology (Oxford, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

15 authors.

Hongjiang LiuDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), Beijing.ORCID 0000-0001-9322-7121
Chun LiDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), Beijing.
Hui ShiDepartment of Rheumatology and Immunology, Shanghai Jiaotong University School of Medicine, Ruijin Hospital, Shanghai, China.
Yixue GuoDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), Beijing.ORCID 0000-0001-6348-5074
Yundi TangDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), Beijing.
Chen ChenDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), Beijing.
Zhen ZhaoDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), Beijing.
Claire K HoyDivision of Rheumatology, University of Michigan, Ann Arbor, MI.
Srilakshmi YalavarthiDivision of Rheumatology, University of Michigan, Ann Arbor, MI.
Gabriel Figueroa-ParraDivision of Rheumatology, Mayo Clinic, Rochester, MN, USA.ORCID 0000-0002-6077-8899
Ali Duarte-GarciaDivision of Rheumatology, Mayo Clinic, Rochester, MN, USA.ORCID 0000-0003-1749-5719
Yu ZuoDivision of Rheumatology, University of Michigan, Ann Arbor, MI.
Zhanguo LiDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), Beijing.
Jason S KnightDivision of Rheumatology, University of Michigan, Ann Arbor, MI.
Jianping GuoDepartment of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), Beijing.

Funding

Thromboinflammatory consequences of infection-induced autoimmunityK08AR080205 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Yu Zuo · 2022 to 2026
$865k
NIAMS NIH HHS K08 AR080205
6 · The paper itself

Abstract

objectiveLeucocyte immunoglobulin-like receptor A3 (LILRA3) belongs to a family of leucocyte receptors. Our previous study reported LILRA3 transcripts were markedly upregulated in neutrophils from patients with APS. We undertook this study to investigate clinical implications of LILRA3 in APS and its potential role in APS-associated thrombosis.

methodsTwo independent cohorts were studied. The first consisted of 294 APS patients, 48 asymptomatic aPL carriers and 150 healthy controls (HCs) from Peking University People's Hospital. The second included 99 APS patients, 25 aPL carriers and 40 HCs from United States APS centres. Serum or plasma concentrations of LILRA3 and MPO-DNA complexes were measured. Additionally, 35 patients with thrombotic APS (tAPS) were evaluated to determine potential effects of immunosuppressive therapy on serum concentrations of LILRA3 and MPO-DNA complexes.

resultsBoth positivity and serum concentration of LILRA3 were significantly increased in APS patients, especially in those with tAPS. LILRA3-positive tAPS patients displayed more severe thrombotic manifestations. Serum LILRA3 was positively correlated with MPO-DNA complexes in LILRA3-positive tAPS. After immunosuppressive treatment, LILRA3 and MPO-DNA complexes were consistently decreased in tAPS patients. Key findings from the Peking cohort were confirmed in the United States cohort.

conclusionOur study provides first evidence that LILRA3 is aberrantly expressed in APS, especially in patients with tAPS. Serum LILRA3 correlated with MPO-DNA complexes, and the two indices were consistently decreased in tAPS patients after treatment. LILRA3 may play a role in thrombosis of APS and may serve as a biomarker and/or therapeutic target in tAPS.

Indexed as

Antiphospholipid SyndromeThrombosisAntibodies, AntiphospholipidBiomarkersCohort StudiesHumansReceptors, ImmunologicAntibodies, AntiphospholipidBiomarkersLILRA3 protein, humanReceptors, ImmunologicAPSclinical relevanceLILRA3thrombosis

Identifiers

PMID35325077
PMCPMC10410100

What Socratic holds

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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.