更新于：2024-11-01

LILRA5

更新于：2024-11-01

基本信息

别名

CD85、CD85 antigen-like family member F、CD85f

+ [10]

简介

May play a role in triggering innate immune responses. Does not seem to play a role for any class I MHC antigen recognition.

关联

项与 LILRA5 相关的药物

HG-1204

靶点

LILRA5

作用机制

LILRA5 modulators

在研机构-

原研机构

Human Genome Sciences, Inc.

在研适应症-

非在研适应症

骨病 [+2]

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 LILRA5 相关的临床结果

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100 项与 LILRA5 相关的转化医学

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0 项与 LILRA5 相关的专利（医药）

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项与 LILRA5 相关的文献（医药）

2024-08-01·Diabetes Research and Clinical Practice

Proteomics profiling and association with cardiorenal complications in type 2 diabetes subtypes in Asian population

Article

作者: Chan, Clara ; Lim, Su Chi ; Sum, Chee Fang ; Lee, Bernett Teck Kwong ; Liu, Jian-Jun ; Zheng, Huili ; Ang, Keven ; Gurung, Resham Lal ; Subramaniam, Tavintharan ; Coffman, Thomas M ; Liu, Sylvia

AIMAmong multi-ethnic Asians, type 2 diabetes (T2D) clustered in three subtypes; mild obesity-related diabetes (MOD), mild age-related diabetes with insulin insufficiency (MARD-II) and severe insulin-resistant diabetes with relative insulin insufficiency (SIRD-RII) had differential cardio-renal complication risk. We assessed the proteomic profiles to identify subtype specific biomarkers and its association with diabetes complications.METHODS1448 plasma proteins at baseline were measured and compared across the T2D subtypes. Multivariable cox regression was used to assess associations between significant proteomics features and cardio-renal complications.RESULTSAmong 645 T2D participants (SIRD-RII [19%], MOD [45%], MARD-II [36%]), 295 proteins expression differed significantly across the groups. These proteins were enriched in cell adhesion, neurogenesis and inflammatory response processes. In SIRD-RII group, ADH4, ACY1, THOP1, IGFBP2, NEFL, ENTPD2, CALB1, HAO1, CTSV, ITGAV, SCLY, EDA2R, ERBB2 proteins significantly associated with progressive CKD and LILRA5 protein with incident heart failure (HF). In MOD group, TAFA5, RSPO3, EDA2R proteins significantly associated with incident HF. In MARD-II group, FABP4 protein significantly associated with progressive CKD and PTPRN2 protein with major adverse cardiovascular events. Genetically determined NEFL and CALB1 were associated with kidney function decline.CONCLUSIONSEach T2D subtype has unique proteomics signature and association with clinical outcomes and underlying mechanisms.

2023-05-01·Cornea

Leukocyte Immunoglobulin-like Receptor A5 Deletion Aggravates the Pathogenesis of Pseudomonas aeruginosa Keratitis by Promoting Proinflammatory Cytokines

Article

作者: Liu, Xi ; Wu, Minhao ; Liang, Siping ; Shang, Yuqi ; Xia, Jinyu ; Wei, Liwen ; Zou, Zhengyu

Purpose:The purpose of this study was to assess the role of leukocyte immunoglobulin-like receptor A5 (LILRA5) in regulating bacterial infection and corneal inflammation.Methods:The human corneal tissue microarray data set GSE58291 from Gene Expression Omnibus was downloaded. Then, the differentially expressed genes, Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, Gene Set Enrichment Analysis, and the immune infiltration analysis were conducted. We constructed the Pseudomonas aeruginosa (P. aeruginosa) keratitis mice model using wild-type and LILRA5-deficient mice. The results of the bioinformatics analysis were verified by the cell in vitro and animal in vivo experiments.Results:This study revealed that LILRA5 is substantially expressed in human keratitis and regulates the immune response negatively. Neutrophils were identified as the core fraction of immune cells in keratitis. After P. aeruginosa infection, neutrophils lacking LILRA5 induced elevated levels of proinflammatory cytokines and toll-like receptor 4. LILRA5 deficiency exacerbated the severity of the infection and the production of proinflammatory cytokines in mice.Conclusions:LILRA5 was discovered as an immunosuppressive regulator in P. aeruginosa keratitis, highlighting its significance in activated immune responses.

2022-09-01·Hepatology

Genome‐wide meta‐analysis identifies susceptibility loci for autoimmune hepatitis type 1

Article

作者: Shi, Junping ; Wang, Xiaoyi ; Wang, Bangmao ; Yuan, Xiaoling ; Tang, Ruqi ; Li, Ke‐Ke ; Sun, Mengying ; Zhang, Xinhe ; Ma, Xiong ; Zhang, Jiming ; Song, Yuhu ; Xu, Jie ; Liu, Yanmin ; Li, Yiling ; Bao, Jie ; Huang, Zuxiong ; Cui, Yong ; Zhou, Yang ; Li, You ; Gershwin, M. Eric ; Ma, Anlin ; Li, Jia ; Hu, Lilin ; Zhou, Lu ; Xiao, Xiao ; Zou, Zhengsheng ; Miao, Qi ; Wang, Qixia ; Zuo, Xianbo ; Wang, Hanxiao ; Du, Shiyu ; Tang, Shanhong ; Zhang, Haiping ; Xu, Yun ; Yang, Ling ; Han, Xu ; Sun, Ying ; Gong, Ling ; Yan, Huiping ; Lian, Min ; Lin, Qiuxiang ; Seldin, Michael F.

AbstractBackground and AimsAutoimmune hepatitis (AIH) is a rare and chronic autoimmune liver disease. While genetic factors are believed to play a crucial role in the etiopathogenesis of AIH, our understanding of these genetic risk factors is still limited. In this study, we aimed to identify susceptibility loci to further understand the pathogenesis of this disease.Approach and ResultsWe conducted a case–control association study of 1,622 Chinese patients with AIH type 1 and 10,466 population controls from two independent cohorts. A meta‐analysis was performed to ascertain variants associated with AIH type 1. A single‐nucleotide polymorphism within the human leukocyte antigen (HLA) region showed the strongest association with AIH (rs6932730: OR = 2.32; p = 9.21 × 10−73). The meta‐analysis also identified two non‐HLA loci significantly associated with AIH: CD28/CTLA4/ICOS on 2q33.3 (rs72929257: OR = 1.31; p = 2.92 × 10−9) and SYNPR on 3p14.2 (rs6809477: OR = 1.25; p = 5.48 × 10−9). In silico annotation, reporter gene assays, and CRISPR activation experiments identified a distal enhancer at 2q33.3 that regulated expression of CTLA4. In addition, variants near STAT1/STAT4 (rs11889341: OR = 1.24; p = 1.34 × 10−7), LINC00392 (rs9564997: OR = 0.81; p = 2.53 × 10−7), IRF8 (rs11117432: OR = 0.72; p = 6.10 × 10−6), and LILRA4/LILRA5 (rs11084330: OR = 0.65; p = 5.19 × 10−6) had suggestive association signals with AIH.ConclusionsOur study identifies two novel loci (CD28/CTLA4/ICOS and SYNPR) exceeding genome‐wide significance and suggests four loci as potential risk factors. These findings highlight the importance of costimulatory signaling and neuro‐immune interaction in the pathogenesis of AIH.