产品号 #70042_C
冻存的人原代细胞
总览
选择即用型、符合伦理的人原代巨噬细胞助您轻松开启实验。我们提供个性化的服务、定制产品、灵活的交付周期，并支持提前测试筛选并预留整个批次，以确保您获得所需的细胞。
通过免疫磁分选的外周血单核细胞培养于添加了10% FBS， M-CSF和IL-4的RPMI 1640中（产品号#36750）培养5天，生成巨噬细胞。IL-4与M-CSF联合可诱导m2a样特性。细胞采集均通过机构审查委员会（IRB）批准的知情同意书及方案进行，并冻存于不含动物成分的CryoStor® CS10冻存液（产品号#07930）中。如有需要，可提供其他文档、高分辨率HLA分型（I类和II类等位基因）以及CMV状态。采集过程中添加酸-柠檬酸-葡萄糖溶液A （ACDA）作为抗凝血剂。选择产品选项后，供体信息（如BMI范围、年龄、种族等）可以在上面的评论框中查询。所有供体均经过HIV-1/2、乙肝和丙肝筛查。
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包含
• CryoStor® CS10
亚型
冻存
细胞类型
巨噬细胞，单核细胞，髓系细胞
种属
人
细胞和组织来源
外周血
供体状态
Normal
纯度
流式细胞术检测：MHC II类+，≥ 90% CD11b+，≥ 90% CD18+，≥ 90% CD68+
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (4)
Publications (2)
TMEM173 Drives Lethal Coagulation in Sepsis. Cell host {\&} microbe 2020
Abstract
The discovery of TMEM173/STING-dependent innate immunity has recently provided guidance for the prevention and management of inflammatory disorders. Here, we show that myeloid TMEM173 occupies an essential role in regulating coagulation in bacterial infections through a mechanism independent of type I interferon response. Mechanistically, TMEM173 binding to ITPR1 controls calcium release from the endoplasmic reticulum in macrophages and monocytes. The TMEM173-dependent increase in cytosolic calcium drives Gasdermin D (GSDMD) cleavage and activation, which triggers the release of F3, the key initiator of blood coagulation. Genetic or pharmacological inhibition of the TMEM173-GSDMD-F3 pathway blocks systemic coagulation and improves animal survival in three models of sepsis (cecal ligation and puncture or bacteremia with Escherichia coli or Streptococcus pneumoniae infection). The upregulation of the TMEM173 pathway correlates with the severity of disseminated intravascular coagulation and mortality in patients with sepsis. Thus, TMEM173 is a key regulator of blood clotting during lethal bacterial infections.
Design of a novel integration-deficient lentivector technology that incorporates genetic and posttranslational elements to target human dendritic cells. Molecular therapy : the journal of the American Society of Gene Therapy 2014 MAR
Abstract
As sentinels of the immune system, dendritic cells (DCs) play an essential role in regulating cellular immune responses. One of the main challenges of developing DC-targeted therapies includes the delivery of antigen to DCs in order to promote the activation of antigen-specific effector CD8 T cells. With the goal of creating antigen-directed immunotherapeutics that can be safely administered directly to patients, Immune Design has developed a platform of novel integration-deficient lentiviral vectors that target and deliver antigen-encoding nucleic acids to human DCs. This platform, termed ID-VP02, utilizes a novel genetic variant of a Sindbis virus envelope glycoprotein with posttranslational carbohydrate modifications in combination with Vpx, a SIVmac viral accessory protein, to achieve efficient targeting and transduction of human DCs. In addition, ID-VP02 incorporates safety features in its design that include two redundant mechanisms to render ID-VP02 integration-deficient. Here, we describe the characteristics that allow ID-VP02 to specifically transduce human DCs, and the advances that ID-VP02 brings to conventional third-generation lentiviral vector design as well as demonstrate upstream production yields that will enable manufacturing feasibility studies to be conducted.
更多信息
| Species | Human |
|---|---|
| Contains | • CryoStor® CS10 |
| Purity | ≥ 90% CD11b+, ≥ 90% CD18+, ≥ 90% CD68+ by flow cytometry, ≥ 90% MHC class II+ |
| Cell And Tissue Source | Peripheral Blood |
| Donor Status | Normal |
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PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.
