更新于：2024-05-01

CD300LF

CD300 molecule like family member f

更新于：2024-05-01

基本信息

别名

CD300 antigen-like family member F、CD300 molecule like family member f、CD300f

+ [11]

简介

Acts as an inhibitory receptor for myeloid cells and mast cells (PubMed:15549731). Positively regulates the phagocytosis of apoptotic cells (efferocytosis) via phosphatidylserine (PS) recognition; recognizes and binds PS as a ligand which is expressed on the surface of apoptotic cells. Plays an important role in the maintenance of immune homeostasis, by promoting macrophage-mediated efferocytosis and by inhibiting dendritic cell-mediated efferocytosis (By similarity). Negatively regulates Fc epsilon receptor-dependent mast cell activation and allergic responses via binding to ceramide and sphingomyelin which act as ligands (PubMed:24035150). May act as a coreceptor for interleukin 4 (IL-4). Associates with and regulates IL-4 receptor alpha-mediated responses by augmenting IL-4- and IL-13-induced signaling (By similarity). Negatively regulates the Toll-like receptor (TLR) signaling mediated by MYD88 and TRIF through activation of PTPN6/SHP-1 and PTPN11/SHP-2 (PubMed:22043923). Inhibits osteoclast formation. Induces macrophage cell death upon engagement (By similarity).

关联

100 项与 CD300LF 相关的临床结果

登录后查看更多信息

100 项与 CD300LF 相关的转化医学

登录后查看更多信息

0 项与 CD300LF 相关的专利（医药）

登录后查看更多信息

119

项与 CD300LF 相关的文献（医药）

2024-01-11·bioRxiv : the preprint server for biology

Murine norovirus mutants adapted to replicate in human cells reveal a post-entry restriction.

作者: Melissa R Budicini ; Valerie J Rodriguez-Irizarry ; Robert W Maples ; Julie K Pfeiffer

RNA viruses lack proofreading in their RNA polymerases and therefore exist as genetically diverse populations. By exposing these diverse viral populations to selective pressures, viruses with mutations that confer fitness advantages can be enriched. To examine factors important for viral tropism and host restriction, we passaged murine norovirus (MNV) in a human cell line, HeLa cells, to select for mutant viruses with increased fitness in non-murine cells. A major determinant of host range is expression of the MNV receptor CD300lf on mouse cells, but additional host factors may limit MNV replication in human cells. We found that viruses passaged six times in HeLa cells had enhanced replication compared with the parental virus. The passaged viruses had several mutations throughout the viral genome, which were primarily located in the viral non-structural coding regions. While viral attachment was not altered for the passaged viruses, their replication was higher than the parental virus when entry was bypassed, suggesting the mutant viruses overcame a post-entry block in human cells. Three mutations in the viral NS1 protein were sufficient for enhanced post-entry replication in human cells. We found that the human cell-adapted MNV variants had reduced fitness in mouse BV2 cells. Although the mutant viruses had increased fitness in HeLa cells, they did not have increased fitness in mice. Overall, this work suggests that MNV tropism is not only determined by the presence of the viral receptor but also post-entry factors.

Importance:

Viruses infect specific species and cell types, which is dictated by expression of host factors required for viral entry as well as downstream replication steps. Murine norovirus (MNV) infects mouse cells, but not human cells. However, human cells expressing the murine CD300lf receptor support MNV replication, suggesting receptor expression is a major determinant of MNV tropism. To determine whether other factors influence MNV tropism, we selected for variants with enhanced replication in human cells. We identified mutations that enhance MNV replication in human cells and demonstrated that these mutations enhance infection at a post-entry replication step. Therefore, MNV infection of human cells is restricted at both entry and post-entry stages. These results shed new light on factors that influence viral tropism and host range.

2023-12-01·COPD

Identification of Potential Differentially-Methylated/Expressed Genes in Chronic Obstructive Pulmonary Disease.

Article

作者: Wen Pan ; Shuyuan An ; Lina Dai ; Shuo Xu ; Dan Liu ; Lizhi Wang ; Ruixue Zhang ; Fengliang Wang ; Zongling Wang

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. DNA methylation can regulate gene expression. Understanding the potential molecular mechanism of COPD is of great importance. The aim of this study was to find differentially methylated/expressed genes in COPD. DNA methylation and gene expression profiles in COPD were downloaded from the dataset, followed by functional analysis of differentially-methylated/expressed genes. The potential diagnostic value of these differentially-methylated/expressed genes was determined by receiver operating characteristic (ROC) analysis. Expression validation of differentially-methylated/expressed genes was performed by in vitro experiment and extra online datasets. Totally, 81 hypermethylated-low expression genes and 121 hypomethylated-high expression genes were found in COPD. Among which, 9 core hypermethylated-low expression genes (CD247, CCR7, CD5, IKZF1, SLAMF1, IL2RB, CD3E, CD7 and IL7R) and 8 core hypomethylated-high expression genes (TREM1, AQP9, CD300LF, CLEC12A, NOD2, IRAK3, NLRP3 and LYZ) were identified in the protein-protein interaction (PPI) network. Moreover, these genes had a potential diagnostic utility for COPD. Some signaling pathways were identified in COPD, including T cell receptor signaling pathway, cytokine-cytokine receptor interaction, hematopoietic cell lineage, HTLV-I infection, endocytosis and Jak-STAT signaling pathway. In conclusion, differentially-methylated/expressed genes and involved signaling pathways are likely to be associated with the process of COPD.

2023-10-20·Cell reports

CD300f immune receptor contributes to healthy aging by regulating inflammaging, metabolism, and cognitive decline.

Article

作者: Frances Evans ; Daniela Alí-Ruiz ; Natalia Rego ; María Luciana Negro-Demontel ; Natalia Lago ; Fabio Andrés Cawen ; Bruno Pannunzio ; Paula Sanchez-Molina ; Laura Reyes ; Andrea Paolino ; Jorge Rodríguez-Duarte ; Valentina Pérez-Torrado ; Almudena Chicote-González ; Celia Quijano ; Inés Marmisolle ; Ana Paula Mulet ; Geraldine Schlapp ; María Noel Meikle ; Mariana Bresque ; Martina Crispo ; Eduardo Savio ; Cristina Malagelada ; Carlos Escande ; Hugo Peluffo

Emerging evidence suggests that immune receptors may participate in many aging-related processes such as energy metabolism, inflammation, and cognitive decline. CD300f, a TREM2-like lipid-sensing immune receptor, is an exceptional receptor as it integrates activating and inhibitory cell-signaling pathways that modulate inflammation, efferocytosis, and microglial metabolic fitness. We hypothesize that CD300f can regulate systemic aging-related processes and ultimately healthy lifespan. We closely followed several cohorts of two strains of CD300f^-/- and WT mice of both sexes for 30 months and observed an important reduction in lifespan and healthspan in knockout mice. This was associated with systemic inflammaging, increased cognitive decline, reduced brain glucose uptake observed by ¹⁸FDG PET scans, enrichment in microglial aging/neurodegeneration phenotypes, proteostasis alterations, senescence, increased frailty, and sex-dependent systemic metabolic changes. Moreover, the absence of CD300f altered macrophage immunometabolic phenotype. Taken together, we provide strong evidence suggesting that myeloid cell CD300f immune receptor contributes to healthy aging.

项与 CD300LF 相关的新闻（医药）

2023-11-28

·Science Daily

Study identifies a key protein for healthy aging

Life expectancy and healthy ageing in mice can be determined by a protein present in some cells of the immune system, according to a new study. When this protein -- known as the CD300f immune receptor -- is absent, animal models have a shorter life expectancy and suffer from pathologies associated with cognitive decline and premature ageing, especially in females. Life expectancy and healthy ageing in mice can be determined by a protein present in some cells of the immune system, according to a study published in the journal Cell Reports. When this protein -- known as the CD300f immune receptor -- is absent, animal models have a shorter life expectancy and suffer from pathologies associated with cognitive decline and premature ageing, especially in females. "Our study indicates that alterations in immune system cells, for instance, in macrophages and microglia, can determine the healthy ageing degree in mice," notes Hugo Peluffo, leader of this study and member of the Faculty of Medicine and Health Sciences and the Institute of Neurosciences (UBneuro) of the University of Barcelona. Understanding how the CD300f immune receptor -- and the myeloid cells of the immune system -- can determine by themselves the onset rate of ageing-associated pathologies, "will help to better understand this process, and it will contribute to the design of strategies to regulate its action. For instance, using the immune receptor CD300f as a target in biomedicine," notes the expert. "Also, our team has previously shown that some variants of the CD300f immune receptor could be useful as biomarkers in patients." The paper, whose first author is the expert Frances Evans (Institute Pasteur and Udelar), includes the participation of teams from the Molecular Imaging Uruguayan Center (CUDIM), among other institutions. What is the role of this receptor in ageing? The CD300f receptor is a protein expressed by immune system cells that modulates cell metabolism and inflammation. This study reveals the first evidence of its role in the processes related to ageing and senescence. "In particular, we discovered that mice that lacked the CD300f immune receptor developed prematurely some pathologies associated with ageing (cognitive deficits, motor incoordination, tumours, etc.) and even damage in several organs such as the brain, the liver or the lungs. Moreover, we observed an important effect on females, the most affected ones," says Hugo Peluffo. The study is based on a detailed monitoring of several cohorts of animals for thirty months, a methodological innovation that allowed the researchers to see the process of real ageing in these animals without using accelerated ageing models, which do not fully represent a process that necessarily involves the gradual accumulation of changes with age. Immune receptors and Alzheimer's disease The researcher points out that "the aim is to keep studying the consequences of the dysfunction of the CD300f immune receptor on brain ageing, in particular on microglia." In these lines, a project led by Professor Hugo Peluffo to study the relationship between ageing and Alzheimer's disease has just received one of the Alzheimer's research grants from the Pasqual Maragall Foundation. It will explore how immune cells in the nervous system, known as microglia, influence the ageing process and the late onset of Alzheimer's. "In this project, funded by the Pasqual Maragall Foundation, we will study the potential role of this immune receptor in Alzheimer's disease," says the researcher.