EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #15624_C
免疫密度梯度离心法去除粒细胞
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专为您的实验方案打造的产品
要查看实验方案所需的所有配套产品，请参阅《实验方案与技术文档》。
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Lymphoprep™Density gradient medium for the isolation of mononuclear cells
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Dulbecco's Phosphate Buffered Saline with 2% ...Cell culture buffer
总览
RosetteSep™人类粒细胞去除混合物从全血中去除粒细胞。四聚体抗体复合物可识别CD66b红细胞（RBC）上的糖蛋白A，从而靶向去除非目的细胞。当在密度梯度介质如Lymphoprep™（产品号 #18060））上进行离心后，非目的细胞会与红细胞一起沉淀。去除粒细胞后的目的细胞为血浆和密度梯度离心液的交界界面中高度富集的细胞。
亚型
细胞分选试剂盒
细胞类型
粒细胞及其亚群
种属
人
样本来源
Buffy Coat，Whole Blood
筛选方法
删除
应用
细胞分选
品牌
RosetteSep
研究领域
免疫
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 (3)
常见问题
文献 (3)
Interleukins 7 and 15 Maintain Human T Cell Proliferative Capacity through STAT5 Signaling. PloS one 2016
Abstract
T lymphocytes require signals from self-peptides and cytokines, most notably interleukins 7 and 15 (IL-7, IL-15), for survival. While mouse T cells die rapidly if IL-7 or IL-15 is withdrawn, human T cells can survive prolonged withdrawal of IL-7 and IL-15. Here we show that IL-7 and IL-15 are required to maintain human T cell proliferative capacity through the STAT5 signaling pathway. T cells from humanized mice proliferate better if stimulated in the presence of human IL-7 or IL-15 or if T cells are exposed to human IL-7 or IL-15 in mice. Freshly isolated T cells from human peripheral blood lose proliferative capacity if cultured for 24 hours in the absence of IL-7 or IL-15. We further show that phosphorylation of STAT5 correlates with proliferation and inhibition of STAT5 reduces proliferation. These results reveal a novel role of IL-7 and IL-15 in maintaining human T cell function, provide an explanation for T cell dysfunction in humanized mice, and have significant implications for in vitro studies with human T cells.
Impaired interferon signaling is a common immune defect in human cancer. Proceedings of the National Academy of Sciences of the United States of America 2009 JUN
Abstract
Immune dysfunction develops in patients with many cancer types and may contribute to tumor progression and failure of immunotherapy. Mechanisms underlying cancer-associated immune dysfunction are not fully understood. Efficient IFN signaling is critical to lymphocyte function; animals rendered deficient in IFN signaling develop cancer at higher rates. We hypothesized that altered IFN signaling may be a key mechanism of immune dysfunction common to cancer. To address this, we assessed the functional responses to IFN in peripheral blood lymphocytes from patients with 3 major cancers: breast cancer, melanoma, and gastrointestinal cancer. Type-I IFN (IFN-alpha)-induced signaling was reduced in T cells and B cells from all 3 cancer-patient groups compared to healthy controls. Type-II IFN (IFN-gamma)-induced signaling was reduced in B cells from all 3 cancer patient groups, but not in T cells or natural killer cells. Impaired-IFN signaling was equally evident in stage II, III, and IV breast cancer patients, and downstream functional defects in T cell activation were identified. Taken together, these findings indicate that defects in lymphocyte IFN signaling arise in patients with breast cancer, melanoma, and gastrointestinal cancer, and these defects may represent a common cancer-associated mechanism of immune dysfunction.
Cell-specific expression and pathway analyses reveal alterations in trauma-related human T cell and monocyte pathways. Proceedings of the National Academy of Sciences of the United States of America 2006 OCT
Abstract
Monitoring genome-wide, cell-specific responses to human disease, although challenging, holds great promise for the future of medicine. Patients with injuries severe enough to develop multiple organ dysfunction syndrome have multiple immune derangements, including T cell apoptosis and anergy combined with depressed monocyte antigen presentation. Genome-wide expression analysis of highly enriched circulating leukocyte subpopulations, combined with cell-specific pathway analyses, offers an opportunity to discover leukocyte regulatory networks in critically injured patients. Severe injury induced significant changes in T cell (5,693 genes), monocyte (2,801 genes), and total leukocyte (3,437 genes) transcriptomes, with only 911 of these genes common to all three cell populations (12%). T cell-specific pathway analyses identified increased gene expression of several inhibitory receptors (PD-1, CD152, NRP-1, and Lag3) and concomitant decreases in stimulatory receptors (CD28, CD4, and IL-2Ralpha). Functional analysis of T cells and monocytes confirmed reduced T cell proliferation and increased cell surface expression of negative signaling receptors paired with decreased monocyte costimulation ligands. Thus, genome-wide expression from highly enriched cell populations combined with knowledge-based pathway analyses leads to the identification of regulatory networks differentially expressed in injured patients. Importantly, application of cell separation, genome-wide expression, and cell-specific pathway analyses can be used to discover pathway alterations in human disease.
更多信息
| 种属 | Human |
|---|---|
| 样本来源 | Buffy Coat, Whole Blood |
| Selection Method | Depletion |
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