Ask about this productRelated genes to: LILRB5 antibody
- Gene:
- LILRB5 NIH gene
- Name:
- leukocyte immunoglobulin like receptor B5
- Previous symbol:
- -
- Synonyms:
- LIR-8, LIR8, CD85c
- Chromosome:
- 19q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-11
- Date modifiied:
- 2016-01-14
Related products to: LILRB5 antibody
Related articles to: LILRB5 antibody
- The mechanisms underlying tumor cell-myeloid cell interactions in the tumor microenvironment (TME) remain unclear, and predictive biomarkers for patient response to myeloid checkpoint blockade are lacking. This study identified specific binding between tight junction claudins (CLDNs) and leukocyte immunoglobulin-like receptor subfamily B2 (LILRB2) and LILRB5. In multiple human cancer cohorts, the spatial proximity of LILRB2-positive macrophages to CLDN-expressing cancer cells correlated with clinical outcomes, highlighting this spatial relationship as a potential biomarker. In syngeneic LILRB2-transgenic and humanized mouse models, CLDN18.2-LILRB2 interactions triggered bidirectional signaling, enhanced the immunosuppressive activity of myeloid cells, and accelerated tumor progression. These effects were reversed by LILRB2 blockade. The CLDN-LILRB2 axis sustained immunosuppression by regulating NF-κB and STAT signaling pathways. Our findings reveal a mechanism of myeloid cell regulation by tight junction proteins in the TME, offering a rationale for targeting this pathway in cancer therapy. - Source: PubMed
Publication date: 2026/04/03
Liu XiaoyeHuang RyanKu ZhiqiangXie JingjingChen HeyuHe YuboLou QiZhang ChengchengYang XingLewis CherylHomsi JadeGupta AnkitDong LeiChen KenianTu AnnabelDu LimingYu HailongHu QingFang MengLi BufanKhan A E M AdanSimith CarolineJohn SamuelXu LinZhang NingyanAn ZhiqiangZhang Cheng Cheng - Genome-wide association studies have identified numerous Alzheimer's disease (AD) susceptibility loci in European populations. However, the genetic architecture of AD in non-European populations remains underinvestigated. - Source: PubMed
Cao HanZheng ZiyuZhou XiaopuKikuchi MasatakaWong Hiu YiCheng Elaine Y LWong Bonnie W YLo Ronnie M NShoai MaryamChong Joyce RChan Andrew L TChen ChristopherLam Linda C WMok Vincent C TKwok Timothy C Y Chen YuIp Fanny C FMok Kin YMiyashita AkinoriIkeuchi TakeshiHardy JohnFu Amy K YIp Nancy Y - Amyloid proteins are linked to various diseases; however, their functional roles in immunity and cancer remain unclear. Here, we establish a direct link between oligomeric cystatin C-a cysteine cathepsin inhibitor and a well-characterized amyloidogenic protein-within the tumor microenvironment and the immune inhibitory receptors LILRB2 and LILRB5 on myeloid cells. We demonstrated that human LILRB2 and LILRB5, along with their murine counterpart PIRB, serve as functional receptors for cystatin C oligomers. Engagement of these inhibitory receptors by oligomeric cystatin C enhances the immunosuppressive activity of myeloid cells, leading to T-cell suppression and tumor progression. Deletion of the CST3 gene, which encodes cystatin C, in host mice and tumor cells impaired tumor growth, whereas its overexpression accelerated cancer progression in LILRB2 and LILRB5 transgenic mice. Mechanistically, cystatin C-LILRB2 signaling is driven by both canonical phosphatases and the enhanced TGF-β pathway. Additionally, we identified interactions between LILRB receptors and transthyretin oligomers, another amyloid linked to transthyretin amyloidosis, suggesting a broader paradigm of amyloid-LILRB interactions. Our findings reveal an unexpected role of oligomeric cystatin C in enhancing myeloid cell immunosuppression, expand the functional spectrum of amyloid proteins and underscore the importance of these proteins in immune evasion and cancer development. - Source: PubMed
Publication date: 2025/11/14
Zhang ChengchengHe YuboLiu XiaoyeXie JingjingFang MengYang XingHuang RyanLou QiLi BufanGupta AnkitLewis CherylDiamond Marc IZhang NingyanAn ZhiqiangZhang Cheng Cheng - Type 2 diabetes (T2D) is a highly heterogeneous disease characterised by subtypes with variations in aetiology, disease progression, and risk of complications. However, potential drug targets for these subtypes have not been explored. This study aims to investigate potential drug targets by integrating proteomics. - Source: PubMed
Publication date: 2025/09/01
Wei JiaheWu HanzhangWang NingjianZhu JiahaoAnjana Ranjit MohanSokolov Aleksandr VSchiöth Helgi BMohan ViswanathanTan Xiao - There are ten leukocyte immunoglobulin (Ig)-like receptor () genes, i.e., five genes encoding activating receptors (, and ) characterized by their truncated cytoplasmic tails, and five genes encoding inhibitory receptors (, and ) characterized by their extended cytoplasmic tails containing immunoreceptor tyrosine-based inhibitory motifs (ITIMs). Among these, , , and are known for harboring high frequencies of copy number variations (CNVs). However, the presence of CNVs in the leukocyte receptor complex (LRC) region complicates single nucleotide polymorphism (SNP) association analysis within commercially available SNP microarray datasets. This study introduces LILR Genotype Imputation with Attribute Bagging (LIBAG), a novel method for determining CNVs in , and from commercially available SNP genotyping array datasets. CNV imputation accuracy peaked at 98.0% for the Infinium Japanese Screening Array, followed by 97.4% for Axiom Japonica V2, 97.3% for Axiom Japonica Array NEO, and 94.3% for Axiom Japonica V1, with the lowest recorded accuracy of 93.6% for the Axiom Genome-wide ASI1 array. For the 1000 Genomes Project (1kGP) dataset, CNV imputation achieved peak accuracies of 94.5% for 1kGP-EAS (East Asian), 86.6% for 1kGP-AMR (Admixed American), 83.8% for 1kGP-EUR European), and 75.0% for 1kGP-AFR (African), particularly after the 20 kb flanking region. Similarly, imputation accuracy for CNV progressively increased, peaking at the 80 kb flanking region. Accuracy reached 1kGP-AMR, reaching 99.2% and 98.9% for 1kGP-AFR, 98.7% for 1kGP-EUR, and 97.5% for 1kGP-EAS. Investigating the copy number (CN) in diseases associated with HLA class I molecules will provide further insights into disease pathogenesis. - Source: PubMed
Publication date: 2025/04/07
Khor Seik-SoonHirayasu KouyukiKawai YosukeKim Hie LimNagasaki MasaoTokunaga Katsushi