Ask about this productRelated genes to: LRRC15 Blocking Peptide
- Gene:
- LRRC15 NIH gene
- Name:
- leucine rich repeat containing 15
- Previous symbol:
- -
- Synonyms:
- LIB
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-25
- Date modifiied:
- 2015-08-27
Related products to: LRRC15 Blocking Peptide
Related articles to: LRRC15 Blocking Peptide
- Pneumonia remains a leading cause of global mortality. Conventional diagnostic approaches frequently fail to distinguish microbial colonization from true infection in the lower respiratory tract, complicating clinical decision-making and contributing to antibiotic overuse. Improved diagnostic strategies are urgently needed. In this prospective, single-center study, deep sputum specimens were collected from patients with respiratory colonization (n = 17) and infectious pneumonia (n = 27) admitted to the neurosurgical ICU of Huashan Hospital. Metagenomic next-generation sequencing (mNGS) and metatranscriptomic profiling were performed to characterize both the pulmonary microbiota and the host immune response. These features were subsequently integrated to construct a diagnostic model. Microbial community profiling revealed reduced alpha diversity and enrichment of metabolically active pathogenic taxa in the infection group, consistent with a dysbiotic state permissive to invasion. In contrast, the colonization group demonstrated a more balanced microbial ecosystem. Transcriptomic analyses identified 2232 differentially expressed host genes between the two groups. The colonization group showed marked activation of the Wnt, MAPK, chemokine, and focal adhesion pathways, which are functionally implicated in epithelial barrier maintenance and early immune homeostasis. A multi-omics diagnostic model incorporating seven gene features (ANKRD52, ZC3HAV1L, SERPINE3, CDPF1, ZNF720, TAGLN3, and LRRC15) achieved a discrimination between colonization and infection (AUC = 0.951 in the training cohort; 0.875 in the validation set). By jointly analyzing the pulmonary microbiome and host transcriptome, this study provides insight into host-microbe interactions distinguishing colonization from infection and presents a predictive model with potential clinical relevance. - Source: PubMed
Publication date: 2026/04/03
Fu ZhangfanSun YuhanYao HaijunLiu QihuiZhang QiranHu JinZhou YangJiang NingAi JingwenJin JialinZhang Wenhong - Microplastics are emerging contaminants that pose health risks. They can cause hepatic lipid interventions, but the underlying mechanisms require investigation. This study assessed the retention of polypropylene microplastics in mouse liver and determined the intercorrelations between hepatic lipid fluctuations and transcriptomic changes. Microplastic-induced liver dysfunction was confirmed by the variations of transamination, cholesterol metabolism, biotransformation, and redox state. Chronic high-dose treatment induced distinct pathological changes, including regional fibrotic remodeling and ultrastructural mitochondrial abnormalities. Raman biospectra of liver slice proposed vital peaks of 1060, 1132, 1168, 1340, 1446, 1618, and 1670 cm, representing the liver biomolecule landscapes. Transcriptomic changes were mainly involved in mRNA transcription, multicellular organism development, various stimuli response, cell differentiation, and lipid metabolic process. Microplastic exposure dosage exerted more profound effects than exposure duration on gene expressions of oxidation-reduction process, signal transduction, and lipid metabolism. WGCNA analysis proposed 47 hub genes involved gene expression orchestration, cell fate monitor, and mitochondria translation modulation. Nine differentially expressed genes associated with lipid biomarkers were related to mitochondria transcription ( and ), cell differentiation , and ), lipid catabolism ( and ) and tRNA methyltransferase (), and Raman peak at 1670 cm intimately connected with aggregated forms of protein. Our findings suggested that polypropylene microplastics could change the liver molecular landscape and induce lipid metabolism disorders and transcriptomic changes in mitochondrial protein translation and expression regulation, highlighting their significant consequences in nutrient and energy imbalance. - Source: PubMed
Publication date: 2025/10/29
Wang MiaoWang JingSun XinglinZhang KenaGao JingXu XiaoyingWu JiaruiTao FangfangZhang DayiLiu Mingying - Immune checkpoint inhibitors show insufficient efficacy against pancreatic ductal adenocarcinoma (PDAC). The tumor microenvironment (TME) has a remarkable influence on responsiveness to cancer immunotherapy. The aim of this study was to investigate immunosuppressive characteristics of TME in PDAC tissues. The flow cytometry (FCM) of PDAC surgical specimens revealed that the profile of tumor-infiltrating leukocytes was classified into myeloid cell- and T-cell-dominant subtypes; the myeloid subtype was associated with poorer patient outcomes. Myeloid-derived suppressor cells (MDSCs) showed the highest hazard ratio among various myeloid cell types. Single-cell RNA sequencing and FCM revealed that most MDSCs, but not lymphocytes, in PDAC tissues characteristically express CD74. Macrophage migration inhibitory factor (MIF), a CD74 ligand, was highly expressed in cancer-associated fibroblasts (CAFs) and cancer cells. Spatial transcriptomics demonstrated that the MIF-CD74 myeloid cell interaction was recognized in CAF-dominant areas in PDAC tissue. CAFs expressing immune suppressor molecules such as MFAP5 and LRRC15 were consistent with MIF CAFs. Furthermore, MIF CAFs enhanced the migratory activity of MDSCs and promoted MDSC induction and activation. In the murine model, MDSCs were significantly increased in MIF-expressing PDAC tumors, as were CD74 M-MDSCs per M-MDSC, confirming in vivo interaction between CD74 and MIF. MDSCs play a crucial role in creating an immunosuppressive TME in PDAC; the MIF-CD74 axis drives interactions between MDSCs and CAFs. - Source: PubMed
Publication date: 2026/02/20
Fukuda HironoriArai KosukeHashimoto EriSekine KeisukeArai YasuhitoHiraoka NobuyoshiHirata AyaYamashita MakikoNarumi KentaKikuchi AyakaSawai EriSawada YuriaSunami AyanaMizoguchi YukihiroSadahiro RyoichiAikawa YukikoHenmi YasukoOkumura GenkiSugiyama EriTakahashi MamiShibata TatsuhiroNishito YukariMizuno HideakiNara SatoshiEsaki MinoruKoyama ShoheiKitano ShigehisaYoshida TeruhikoOchiai AtsushiTsunoda HiroyukiAoki Kazunori - Joint function is impaired by disuse, as well as overuse. However, the underlying mechanisms remain unclear. Here, we elucidate the mechanisms of synovial and cartilage changes using a minimized mechanical stress (MMS) mouse model by combining knee joint immobilization and unloading. In this model, synovitis appeared by day 3, followed by subsequent fibrosis leading to joint contracture within two weeks. In contrast, articular cartilage degeneration developed gradually after the synovial alterations. Notably, synovial changes were attenuated by discontinuation of joint immobilization, while cartilage changes improved after discontinuation of joint immobilization and loading. Bulk RNA sequencing (RNA-seq) analyses supported the transcriptomic alterations for synovitis, fibrosis, and cartilage degeneration, and identified ten cytokines associated with cartilage changes. Single-cell RNA-seq (scRNA-seq) further identified distinct subsets in the MMS synovium: Lrrc15 myofibroblasts and Mmp9 macrophages, expressing many of these cytokines. Histological examination showed that MMS initially induced macrophage proliferation, while macrophage depletion by intra-articular administration of clodronate liposomes inhibited MMS-induced synovitis, fibrosis and cartilage degeneration, accompanied by a marked reduction in the MMS-distinct subsets. Our findings identified MMS-induced alterations in synovial cells and their roles in joint phenotype, suggesting that joint motion and mechanical loading contribute to the regulation of joint homeostasis. - Source: PubMed
Publication date: 2026/02/09
Ishikura HisatoshiOkada HiroyukiKin YotaChijimatsu RyotaHiguchi JunyaMiyahara JunyaTachibana NaohiroNagata KoseiTerashima AsukaYano FumikoOmata YasunoriSeki MasahideSuzuki YutakaBaron RolandTanaka SakaeSaito Taku - Chimeric antigen receptor (CAR) T-cell therapy offers a promising approach to improve outcomes for patients with relapsed, refractory, or metastatic osteosarcoma. However, novel target antigens are needed to overcome obstacles limiting CAR T-cell efficacy against osteosarcoma and other solid tumors. Leucine-rich repeat-containing 15 (LRRC15) has been identified as a promising target in patients with osteosarcoma. Given these findings, we aimed to develop LRRC15-CAR T cells and evaluate their antitumor activity and safety in preclinical models. - Source: PubMed
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