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    LILRA3 leukocyte immunoglobulin like receptor A3 [ Homo sapiens (human) ]

    Gene ID: 11026, updated on 11-Apr-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Leukocyte Ig-like receptor A3 facilitates inflammation, migration and invasion of synovial tissue-derived fibroblasts via ERK/JNK activation.

    Leukocyte Ig-like receptor A3 facilitates inflammation, migration and invasion of synovial tissue-derived fibroblasts via ERK/JNK activation.
    Liu M, Tang Y, Du Y, Zhang J, Hu F, Zou Y, Li Y, Zhu L, He J, Guo J, Li Z.

    03/5/2024
    Leukocyte immunoglobulin-like receptor A3 gene deletion in five Chinese populations and protective association with nasopharyngeal carcinoma.

    Leukocyte immunoglobulin-like receptor A3 gene deletion in five Chinese populations and protective association with nasopharyngeal carcinoma.
    Tian W, Li LX, Cheng W, Jin HK, Zhang SS.

    01/15/2024
    Soluble LILRA3 is aberrantly expressed in antiphospholipid syndrome (APS) and is a potential marker of thrombotic APS.

    Soluble LILRA3 is aberrantly expressed in antiphospholipid syndrome (APS) and is a potential marker of thrombotic APS.
    Liu H, Li C, Shi H, Guo Y, Tang Y, Chen C, Zhao Z, Hoy CK, Yalavarthi S, Figueroa-Parra G, Duarte-Garcia A, Zuo Y, Li Z, Knight JS, Guo J., Free PMC Article

    12/3/2022
    A susceptibility locus in the IL12B but not LILRA3 region is associated with vascular damage in Takayasu arteritis.

    A susceptibility locus in the IL12B but not LILRA3 region is associated with vascular damage in Takayasu arteritis.
    Kadoba K, Watanabe R, Iwasaki T, Nakajima T, Kitagori K, Akizuki S, Murakami K, Nakashima R, Hashimoto M, Tanaka M, Ohmura K, Morinobu A, Terao C, Yoshifuji H., Free PMC Article

    11/13/2021
    Leukocyte immunoglobulin-like receptor A3 is increased in IBD patients and functions as an anti-inflammatory modulator.

    Leukocyte immunoglobulin-like receptor A3 is increased in IBD patients and functions as an anti-inflammatory modulator.
    Lan X, Liu F, Ma J, Chang Y, Lan X, Xiang L, Shen X, Zhou F, Zhao Q., Free PMC Article

    08/21/2021
    Association of the Leukocyte Immunoglobulin-like Receptor A3 Gene With Neutrophil Activation and Disease Susceptibility in Adult-Onset Still's Disease.

    Association of the Leukocyte Immunoglobulin-like Receptor A3 Gene With Neutrophil Activation and Disease Susceptibility in Adult-Onset Still's Disease.
    Wang M, Liu M, Jia J, Shi H, Teng J, Liu H, Sun Y, Cheng X, Ye J, Su Y, Chi H, Liu T, Wang Z, Wan L, Meng J, Ma Y, Yang C, Hu Q., Free PMC Article

    08/14/2021
    in systemic lupus erythematosus serum level elevated and correlated with disease activity and severity

    The expression and clinical significance of different forms of LILRA3 in systemic lupus erythematosus.
    Du Y, Sun F, Zhou M, Wu X, Sun W, Jiang Y, Cheng Q, Chen X, Wu H, Xue J.

    04/4/2020
    Study found possible protective effect of the T allele of LILRB1 rs1061680:T>C and no association with insertion/deletion polymorphisms of LILRA3 with ankylosing spondylitis (AS)

    The effect of LILRB1 but not LILRA3 gene polymorphism in immunopathology of ankylosing spondylitis-A parallel to KIR genes.
    Majorczyk E, Wiśniewski A, Zoń-Giebel A, Chlebicki A, Wiland P, Kuśnierczyk P.

    12/14/2019
    LILRA3 polymorphism is associated with Takayasu arteritis.

    Genetic determinants and an epistasis of LILRA3 and HLA-B*52 in Takayasu arteritis.
    Terao C, Yoshifuji H, Matsumura T, Naruse TK, Ishii T, Nakaoka Y, Kirino Y, Matsuo K, Origuchi T, Shimizu M, Maejima Y, Amiya E, Tamura N, Kawaguchi T, Takahashi M, Setoh K, Ohmura K, Watanabe R, Horita T, Atsumi T, Matsukura M, Miyata T, Kochi Y, Suda T, Tanemoto K, Meguro A, Okada Y, Ogimoto A, Yamamoto M, Takahashi H, Nakayamada S, Saito K, Kuwana M, Mizuki N, Tabara Y, Ueda A, Komuro I, Kimura A, Isobe M, Mimori T, Matsuda F., Free PMC Article

    02/23/2019
    Mutations in the genes glucokinase regulatory protein (GCKR), RNase L (RNASEL), leukocyte immunoglobulin-like receptor 3 (LILRA3), and dynein axonemal heavy chain 10 (DNAH10) segregated with elevated HDLc levels in families, while no mutations associated with low HDLc.

    Identification of four novel genes contributing to familial elevated plasma HDL cholesterol in humans.
    Singaraja RR, Tietjen I, Hovingh GK, Franchini PL, Radomski C, Wong K, vanHeek M, Stylianou IM, Lin L, Wang L, Mitnaul L, Hubbard B, Winther M, Mattice M, Legendre A, Sherrington R, Kastelein JJ, Akinsanya K, Plump A, Hayden MR., Free PMC Article

    01/13/2018
    The homozygous LILRA3 deletion is associated with a higher susceptibility for HIV disease and with a faster disease progression.

    LILRA3 deletion is a genetic risk factor of HIV infection.
    Ahrenstorf G, Low HZ, Kniesch K, Ordonez D, Meyer-Olson D, Ahmad F, Kücherer C, Gunsenheimer-Bartmeyer B, Stoll M, Matthias T, Schmidt RE, Witte T.

    12/23/2017
    Letter: LILRA3 gene deletion is not involved in the giant cell arteritis and systemic sclerosis predisposition in Spanish patients.

    LILRA3 deficiency is not involved in the giant cell arteritis and systemic sclerosis predisposition.
    Márquez A, Fernández-Aranguren T, Witte T, González-Gay MA, Martín J, Spanish GCA Group, Spanish Scleroderma Group.

    01/28/2017
    LILRA3 significantly reversed Nogo-66-mediated inhibition of neurite outgrowth and promoted synapse formation in primary cortical neurons through regulation of the ERK/MEK pathway.

    Soluble LILRA3 promotes neurite outgrowth and synapses formation through a high-affinity interaction with Nogo 66.
    An H, Brettle M, Lee T, Heng B, Lim CK, Guillemin GJ, Lord MS, Klotzsch E, Geczy CL, Bryant K, Fath T, Tedla N.

    01/14/2017
    Experiments point towards a beneficial role for LILRA3 in virus infections, especially in ssRNA viruses, like HIV, that engage TLR8; however, the potentially beneficial role of LILRA3 is abrogated during a HIV infection.

    TLR8 regulation of LILRA3 in monocytes is abrogated in human immunodeficiency virus infection and correlates to CD4 counts and virus loads.
    Low HZ, Ahrenstorf G, Pommerenke C, Habermann N, Schughart K, Ordóñez D, Stripecke R, Wilk E, Witte T., Free PMC Article

    10/22/2016
    LILRA3 gene deletion was not associated with Multiple Sclerosis susceptibility and did not affect the age of disease onset, clinical subtype or disease severity.

    Serum Leukocyte Immunoglobulin-Like Receptor A3 (LILRA3) Is Increased in Patients with Multiple Sclerosis and Is a Strong Independent Indicator of Disease Severity; 6.7kbp LILRA3 Gene Deletion Is Not Associated with Diseases Susceptibility.
    An H, Lim C, Guillemin GJ, Vollmer-Conna U, Rawlinson W, Bryant K, Tedla N., Free PMC Article

    07/30/2016
    Evidence showed lack of significant association between LILRA3 deletion and multiple sclerosis pathogenesis. [meta-analysis]

    Influence of the LILRA3 Deletion on Multiple Sclerosis Risk: Original Data and Meta-Analysis.
    Ortiz MA, Núñez C, Ordóñez D, Alvarez-Cermeño JC, Martínez-Rodriguez JE, Sánchez AJ, Arroyo R, Izquierdo G, Malhotra S, Montalban X, García-Merino A, Munteis E, Alcina A, Comabella M, Matesanz F, Villar LM, Urcelay E., Free PMC Article

    05/14/2016
    LILRA3 is a new susceptibility factor for systemic lupus erythematosus (SLE) and primary Sjogren's syndrome (pSS). It predisposes to certain phenotypes such as leucopenia, thrombocytopenia, autoantibody positivity and increased disease activity.

    Impact of the leucocyte immunoglobulin-like receptor A3 (LILRA3) on susceptibility and subphenotypes of systemic lupus erythematosus and Sjögren's syndrome.
    Du Y, Su Y, He J, Yang Y, Shi Y, Cui Y, Luo C, Wu X, Liu X, Hu F, Ma X, Zheng L, Zhang J, Zuo X, Sheng Y, Wu L, Zhang X, Guo J, Li Z.

    01/16/2016
    The current study was conducted to investigate the association of rs103294 of LILRA3 with benign prostatic hyperplasia risk.

    LILRA3 is associated with benign prostatic hyperplasia risk in a Chinese Population.
    Jiao Y, Wang L, Gu X, Tao S, Tian L, Na R, Chen Z, Kang J, Zheng SL, Xu J, Sun J, Qi J., Free PMC Article

    10/3/2015
    ILT6 deletion polymorphism does not appear to be a lupus susceptibility gene in South Indian Tamils, but may behave as a genetic modifier of autoantibody phenotype by influencing the production of anti-Ro60 and anti-Ro52 autoantibodies

    Immunoglobulin-like transcripts 6 (ILT6) polymorphism influences the anti-Ro60/52 autoantibody status in South Indian SLE patients.
    Devaraju P, Witte T, Schmidt RE, Gulati R, Negi VS.

    05/16/2015
    LILRA3 is an immunostimulatory molecule, whose deficiency is associated with higher frequency of B-non-Hodgkin's lymphoma.

    Association of the LILRA3 deletion with B-NHL and functional characterization of the immunostimulatory molecule.
    Low HZ, Reuter S, Topperwien M, Dankenbrink N, Peest D, Kabalak G, Stripecke R, Schmidt RE, Matthias T, Witte T., Free PMC Article

    08/9/2014
    functional LILRA3 is a novel genetic risk factor for rheumatoid arthritis (RA), especially in males. It appears to highly predispose to ACPA-positive RA and confers an increased risk of disease severity in patients with early RA.

    Contribution of functional LILRA3, but not nonfunctional LILRA3, to sex bias in susceptibility and severity of anti-citrullinated protein antibody-positive rheumatoid arthritis.
    Du Y, Cui Y, Liu X, Hu F, Yang Y, Wu X, Liu X, Ma X, Zuo X, Sheng Y, Liu X, Xu J, Zhu P, Sun L, Hong N, Zhang X, Guo J, Li Z.

    06/14/2014
    Data did not indicate any association of LILRA3 deletion with multiple sclerosis (MS) susceptibility, however, patients negative for the deletion may begin to suffer from MS significantly earlier than patients who are positive.

    6.7-kbp deletion in LILRA3 (ILT6) gene is associated with later onset of the multiple sclerosis in a Polish population.
    Wiśniewski A, Wagner M, Nowak I, Bilińska M, Pokryszko-Dragan A, Jasek M, Kuśnierczyk P.

    08/31/2013
    LILRA3 binds both classical and non-classical HLA class I molecules but with reduced affinities compared to LILRB1/LILRB2

    LILRA3 binds both classical and non-classical HLA class I molecules but with reduced affinities compared to LILRB1/LILRB2: structural evidence.
    Ryu M, Chen Y, Qi J, Liu J, Fan Z, Nam G, Shi Y, Cheng H, Gao GF., Free PMC Article

    12/3/2011
    LILRA1 and LILRA3 generally display a greater binding preference for binding to HLA-C free heavy chain, particularly following removal of beta2-microglobulin by acid treatment.

    HLA class I allelic sequence and conformation regulate leukocyte Ig-like receptor binding.
    Jones DC, Kosmoliaptsis V, Apps R, Lapaque N, Smith I, Kono A, Chang C, Boyle LH, Taylor CJ, Trowsdale J, Allen RL.

    05/21/2011
    These results suggest that LILRA3 may play a role in chronic inflammatory conditions such as rheumatoid arthritis.

    Soluble LILRA3, a potential natural antiinflammatory protein, is increased in patients with rheumatoid arthritis and is tightly regulated by interleukin 10, tumor necrosis factor-alpha, and interferon-gamma.
    An H, Chandra V, Piraino B, Borges L, Geczy C, McNeil HP, Bryant K, Tedla N.

    11/13/2010
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