EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #10961_C
人单核细胞向巨噬细胞分化的无血清培养基
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总览
ImmunoCult™-SF巨噬细胞培养基用于搭配适当的细胞因子和刺激剂进行人单核细胞体外培养和向巨噬细胞分化。Immunocult™-SF巨噬细胞培养基中不包含巨噬细胞分化和活化因子，以便用户灵活地制备满足其要求的完全培养基。该培养基是一种专门的无血清培养基，可用于在6或8天周期的人单核细胞向M1（经典活化）和M2a（非传统活化）巨噬细胞分化。
包含
• Iscove’s MDM
• 预检牛血清白蛋白
• 重组人胰岛素
• 人转铁蛋白（铁饱和）
• 2-巯基乙醇
• 添加物
分类
专用培养基
细胞类型
巨噬细胞，单核细胞
种属
人
应用
细胞培养，分化
品牌
ImmunoCult
研究领域
药物发现和毒性检测，免疫学，传染病
制剂类别
无血清
实验数据
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (11)
文献 (8)
The Vi Capsular Polysaccharide of Salmonella Typhi Promotes Macrophage Phagocytosis by Binding the Human C-Type Lectin DC-SIGN.
mBio 2022 dec
Abstract
Capsular polysaccharides are common virulence factors of extracellular,but not intracellular bacterial pathogens,due to the antiphagocytic properties of these surface structures. It is therefore paradoxical that Salmonella enterica subspecies enterica serovar Typhi,an intracellular pathogen,synthesizes a virulence-associated (Vi) capsule,which exhibits antiphagocytic properties. Here,we show that the Vi capsular polysaccharide has different functions when S. Typhi interacts with distinct subsets of host phagocytes. The Vi capsular polysaccharide allowed S. Typhi to selectively evade phagocytosis by human neutrophils while promoting human macrophage phagocytosis. A screen of C-type lectin receptors identified human DC-SIGN as the receptor involved in macrophage binding and phagocytosis of capsulated S. Typhi. Consistent with the anti-inflammatory activity of DC-SIGN,purified Vi capsular polysaccharide reduced inflammatory responses in macrophages. These data suggest that binding of the human C-type lectin receptor DC-SIGN by the Vi capsular polysaccharide contributes to the pathogenesis of typhoid fever. IMPORTANCE Salmonella enterica subspecies enterica serovar Typhi is the causative agent of typhoid fever. The recent emergence of S. Typhi strains which are resistant to antibiotic therapy highlights the importance of vaccination in managing typhoid fever. The virulence-associated (Vi) capsular polysaccharide is an effective vaccine against typhoid fever,but the role the capsule plays during pathogenesis remains incompletely understood. Here,we identify the human C-type lectin receptor DC-SIGN as the receptor for the Vi capsular polysaccharide. Binding of capsulated S. Typhi to DC-SIGN resulted in phagocytosis of the pathogen by macrophages and induction of an anti-inflammatory cytokine response. Thus,the interaction of the Vi capsular polysaccharide with human DC-SIGN contributes to the pathogenesis of typhoid fever and should be further investigated in the context of vaccine development.
Interaction of chikungunya virus glycoproteins with macrophage factors controls virion production
The EMBO Journal 2024 Sep
Abstract
Despite their role as innate sentinels,macrophages can serve as cellular reservoirs of chikungunya virus (CHIKV),a highly-pathogenic arthropod-borne alphavirus that has caused large outbreaks among human populations. Here,with the use of viral chimeras and evolutionary selection analysis,we define CHIKV glycoproteins E1 and E2 as critical for virion production in THP-1 derived human macrophages. Through proteomic analysis and functional validation,we further identify signal peptidase complex subunit 3 (SPCS3) and eukaryotic translation initiation factor 3 subunit K (eIF3k) as E1-binding host proteins with anti-CHIKV activities. We find that E1 residue V220,which has undergone positive selection,is indispensable for CHIKV production in macrophages,as its mutation attenuates E1 interaction with the host restriction factors SPCS3 and eIF3k. Finally,we show that the antiviral activity of eIF3k is translation-independent,and that CHIKV infection promotes eIF3k translocation from the nucleus to the cytoplasm,where it associates with SPCS3. These functions of CHIKV glycoproteins late in the viral life cycle provide a new example of an intracellular evolutionary arms race with host restriction factors,as well as potential targets for therapeutic intervention.
Adipocyte inflammation is the primary driver of hepatic insulin resistance in a human iPSC-based microphysiological system
Nature Communications 2024 Sep
Abstract
Interactions between adipose tissue,liver and immune system are at the center of metabolic dysfunction-associated steatotic liver disease and type 2 diabetes. To address the need for an accurate in vitro model,we establish an interconnected microphysiological system (MPS) containing white adipocytes,hepatocytes and proinflammatory macrophages derived from isogenic human induced pluripotent stem cells. Using this MPS,we find that increasing the adipocyte-to-hepatocyte ratio moderately affects hepatocyte function,whereas macrophage-induced adipocyte inflammation causes lipid accumulation in hepatocytes and MPS-wide insulin resistance,corresponding to initiation of metabolic dysfunction-associated steatotic liver disease. We also use our MPS to identify and characterize pharmacological intervention strategies for hepatic steatosis and systemic insulin resistance and find that the glucagon-like peptide-1 receptor agonist semaglutide improves hepatocyte function by acting specifically on adipocytes. These results establish our MPS modeling the adipose tissue-liver axis as an alternative to animal models for mechanistic studies or drug discovery in metabolic diseases. In vitro modelling of the adipose tissue-liver axis can advance understanding and therapy of metabolic disease,including by distinguishing effects of obesity and inflammation. Here,authors develop such a system based on isogenic human iPSCs and interconnected microphysiological devices.
更多信息
| 物种 | 人 |
|---|---|
| Contains | • Iscove’s MDM • Pre-tested bovine serum albumin • Recombinant human insulin • Human transferrin (iron-saturated) • 2-Mercaptoethanol • Supplements |
| 配方 | 无血清 |
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