Proteins LAIR1 , Human
- Known as:
- Proteins LAIR1 , Human
- Catalog number:
- C368
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins LAIR1 Human
Related genes to: Proteins LAIR1 , Human
- Gene:
- LAIR1 NIH gene
- Name:
- leukocyte associated immunoglobulin like receptor 1
- Previous symbol:
- -
- Synonyms:
- CD305
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2016-10-05
Related products to: Proteins LAIR1 , Human
Related articles to: Proteins LAIR1 , Human
- Acute myeloid leukemia (AML) is a hematologic malignancy with high relapse rates and limited treatment options due to extensive intra-tumor heterogeneity across patients. To characterize this heterogeneity, we profiled matched bone marrow mononuclear cell (BMMC) samples from 26 patients with adult AML at diagnosis and relapse using the cellular indexing of transcriptome and epitope sequencing (CITE-seq) and quantitative flow cytometry. These data together represent a comprehensive multimodal and longitudinal single-cell resource that reveals the transcriptomic and immunophenotypic landscape of AML. Data integration of CITE-seq and flow cytometry surface antigen readouts enabled systematic quantitation of surface antigen co-expression across individual leukemic cells, providing a granular framework for the design of immunotherapeutic strategies to target heterogeneous AML. With this resource, we identified CD33, CLL-1, LAIR1, ITGA4, DEC-205, and CD244 as antigens that induced cytotoxicity in AML cell lines when co-targeted by antibody drug conjugates (ADCs) or chimeric antigen receptor T (CAR-T) cells, demonstrating the exploitation of AML heterogeneity for immunotherapeutic innovation. - Source: PubMed
Publication date: 2026/03/11
Ung MatthewEtchin JuliaHalfond AmandaDiFazio JuliaKeschner YoninaPyclik AlyssaCampbell AnneWang RuijiaSilva MarianaGjeci BrikenaMontalbano AntoninoWilliams ReidMundelboim GuyArruda AndreaMinden MarkScherer JulianChakraborty TirthaGe Huanying GaryLydeard John R - C-reactive protein (CRP) plays dual roles in influenza infection, contributing to immune protection but potentially exacerbating severe outcomes. - Source: PubMed
Publication date: 2026/03/09
Luo JunhaoZhang ZhuohanZhao SongPu SiyuLi LiGao Rongbao - Checkpoint blockade of PD-1 with pembrolizumab provides long-term survival to a significant proportion of patients with metastatic melanoma. Pembrolizumab has been successfully used in combination with chemotherapy in non-small-cell lung cancer to increase the response rate. This phase II trial combined pembrolizumab with carboplatin/paclitaxel (CP) to assess its safety and efficacy, and to identify correlates of responses. Thirty patients without prior immunotherapy for unresectable/metastatic melanoma were treated with pembrolizumab and CP. Peripheral blood was collected at baseline and after 2 cycles to characterize systemic immune activity by multiplex assays and flow cytometry. Seventy percent of patients received all 4 cycles of CP; 87% received pembrolizumab for 2 y or until progression. Grade 3 and higher adverse events (AEs) occurred in 50% of the patients. The overall response rate (ORR) and disease control rate (DCR) by irRC criteria were 43% and 53%, respectively. Median overall survival (OS) was 23.8 months. Objective response was associated with a lower frequency of naive CD8 T cells and low plasma CCL3 at baseline, along with a larger proportion of mature NK cells and of CD4 T cells expressing BTLA or LAIR-1. Survival rate was higher for patients with lower baseline of IL-6, IL-8, and CD4CD39 T cells. Following treatment, pro-inflammatory soluble factors increased in both responders and non-responders. Addition of CP to pembrolizumab in this study did not appear to result in a response or survival advantage and was less tolerable than immunotherapy alone. Correlative data point to peripheral signals to investigate further as potential biomarkers. Trial registration: clinicaltrials.gov, NCT02617849, registered on December 1st, 2015. - Source: PubMed
Publication date: 2026/02/24
Lambert CarolineJamal RahimaThébault PamélaCocolakis EftihiaBélanger KarlDionne JeanneCailhier Jean-FrançoisLe HuyLetendre CarolineLepage StéphanieShechtman YelenaLapointe RéjeanMiller Wilson H - Visceral adiposity tissue (VAT), fat located within the abdominal cavity, may play a causal role in driving inflammation and poor cardiometabolic health. This study investigates the cross-sectional relationships between multiple cardiometabolic traits, including VAT, and proteomic-based inflammatory signatures. Body adiposity distribution quantified using dual-energy X-ray absorptiometry (DXA), cardiometabolic traits, and plasma proteomics inflammation panel (Olink Explore 384) were measured in a discovery cohort from the Vitamin D and Omega-3 Trial (VITAL; N = 525) and a replication cohort from the Cocoa Supplement and Multivitamin Outcomes Study (COSMOS; N = 371). We derived inflammatory proteomic markers of VAT, systolic blood pressure (SBP), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), fasting glucose, and insulin resistance (Homeostasis Model Assessment of Insulin Resistance; HOMA-IR). Inflammatory proteomic markers were identified via linear regression at a false discovery rate (FDR) < 0.05. Proteomic markers showed aligned associations with VAT and the other cardiometabolic traits, except for HDL-C, which was opposite. After adjusting for VAT levels, most proteomic markers were no longer statistically significant: >97% for glucose and SBP, and 73%, 62%, and 56% for HOMA-IR, TG, and HDL-C, respectively, suggesting that VAT explains the variability of these associations. To further elucidate shared mechanisms, we examined the network architecture of 86 proteomic markers common to all cardiometabolic traits. Some of the VAT-dependent protein signatures with high centrality were TGFB1, PDLIM7, COLEC12, and LAIR1. These hub-like proteins may reflect the influence of VAT accumulation on other cardiometabolic traits and highlight novel therapeutic targets for reducing cardiometabolic risk. - Source: PubMed
Publication date: 2025/12/25
Yazdani AzamWang CongDemler OlgaOsifala OluwafeyisolaGiovannucci EdwardZhang HongTobias Deirdre K - LAIR-1 is an inhibitory receptor on immune cells that recognizes collagens and collagen domain-containing proteins. The high abundance of both LAIR-1 and its ligands suggests tight regulation of this interaction. MARCO is a scavenger receptor with a collagen-like domain that is highly expressed on immunosuppressive macrophages. Here, we identified MARCO as a ligand for LAIR-1. MARCO interacted with LAIR-1 in trans and induced inhibitory signaling by LAIR-1 in human natural killer (NK) cells. MARCO and LAIR-1 were coexpressed by human macrophages in tumors and after stimulation of monocyte-derived macrophages with the cytokine interleukin-10 (IL-10) in vitro. Single-molecule fluorescence microscopy demonstrated that MARCO and LAIR-1 interacted in cis on THP-1 macrophages. Whereas the interaction did not affect the scavenger function of MARCO on human macrophages, it reduced both LAIR-1 binding and the LAIR-1 signaling response to collagen. LAIR-1-mediated inhibitory function was increased after CRISPR-Cas9-mediated knockout of MARCO in IL-10-polarized primary human monocyte-derived macrophages. Our results identify MARCO as a regulator of LAIR-1 signaling and suggest that the induction of MARCO on immunosuppressive macrophages could enhance their function by releasing LAIR-1-mediated inhibition. - Source: PubMed
Publication date: 2025/12/09
Singh AkashdipVijver Saskia VAglmous-Talibi HajarJukic NebojsaChen PeirongCrawley SuzanneMondal KalyaniZhou JingNiederauer ChristianMatharu ZimpleLi BettyFan Binvan der Vlist MichielKaplan Daniel DRivera Lee BSissons JamesSitrin JonathanGanzinger Kristina AInês Pascoal Ramos MMeyaard Linde