EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #10970_C
人T细胞激活扩增试剂
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总览
该产品可在无磁珠、无饲养细胞及无抗原条件下实现人 T 细胞的高效激活与扩增。
温和的刺激方式可保持较高的细胞活性，激活后的 T 细胞可进一步在 ImmunoCult™-XF T Cell Expansion Medium（产品号#10981）或其他培养基中扩增。ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator 由可溶性抗体复合物组成，可同时结合并交联 CD3、CD28 和 CD2 受体，提供 T 细胞激活所需的初始及共刺激信号。
该产品适用于科研用途；若用于细胞治疗生产，请选用在相关 GMP 条件下制备的 ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator（产品号#100-0785）。
包含
• 抗人CD3单特异性抗体复合物
• 抗人CD28单特异性抗体复合物
• 抗人CD2单特异性抗体复合物
分类
添加剂
细胞类型
T 细胞，T 细胞，CD4+，T 细胞，CD8+
种属
人
应用
激活，细胞培养，扩增
品牌
ImmunoCult
研究领域
免疫，细胞治疗开发
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 (23)
文献 (29)
LFA-1 integrin antibodies inhibit leukocyte α4β1-mediated adhesion by intracellular signaling.
Blood 2016 JUL
Abstract
Binding of ICAM-1 (intercellular adhesion molecule-1) to the β2-integrin LFA-1 (leukocyte function associated antigen-1) is known to induce crosstalk to the α4β1 integrin. Using different LFA-1 monoclonal antibodies we have been able to study the requirement and mechanism of action for the crosstalk in considerable detail. LFA-1 activating antibodies and those inhibitory antibodies that signal to α4β1 induce phosphorylation of Thr-758 on the β2-chain,which is followed by binding of 14-3-3 proteins and signaling through the G protein exchange factor Tiam1. This results in dephosphorylation of Thr-788/789 on the β1-chain of α4β1 and loss of binding to its ligand VCAM-1 (vascular cell adhesion molecule-1). The results show that with LFA-1 antibodies,we can either 1) activate LFA-1 and inhibit α4β1,2) inhibit both LFA-1 and α4β1,3) inhibit LFA-1 but not α4β1 or 4) not affect LFA-1 or α4β1 These findings are important for the understanding of integrin regulation and for the interpretation of the effect of integrin antibodies and their use in clinical applications.
PD-1+ melanocortin receptor dependent-Treg cells prevent autoimmune disease.
Scientific reports 2019 nov
Abstract
Experimental autoimmune uveoretinitis (EAU) is a mouse model of human autoimmune uveitis marked by ocular autoantigen-specific regulatory immunity in the spleen. The melanocortin 5 receptor (MC5r) and adenosine 2 A receptor (A2Ar) are required for induction of post-EAU regulatory T cells (Tregs) which provide resistance to EAU. We show that blocking the PD-1/PD-L1 pathway prevented suppression of EAU by post-EAU Tregs. A2Ar induction of PD-1+FoxP3+ Tregs in uveitis patients was similar compared to healthy controls,but was significantly reduced with melanocortin stimulation. Further,lower body mass index correlated with responsiveness to stimulation of this pathway. These observations indicate an importance of the PD-1/PD-L1 pathway to provide resistance to relapsing uveitis and shows a reduced capacity of uveitis patients to induce Tregs when stimulated through melanocortin receptors,but that it is possible to bypass this part of the pathway through direct stimulation of A2Ar.
Myalgic encephalomyelitis/chronic fatigue syndrome patients exhibit altered T cell metabolism and cytokine associations.
The Journal of clinical investigation 2019 dec
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease with no known cause or mechanism. There is an increasing appreciation for the role of immune and metabolic dysfunction in the disease. ME/CFS has historically presented in outbreaks,often has a flu-like onset,and results in inflammatory symptoms. Patients suffer from severe fatigue and post-exertional malaise. There is little known about the metabolism of specific immune cells in ME/CFS patients. To investigate immune metabolism in ME/CFS,we isolated CD4+ and CD8+ T cells from 53 ME/CFS patients and 45 healthy controls. We analyzed glycolysis and mitochondrial respiration in resting and activated T cells,along with markers related to cellular metabolism,and plasma cytokines. We found that ME/CFS CD8+ T cells have reduced mitochondrial membrane potential compared to healthy controls. Both CD4+ and CD8+ T cells from ME/CFS patients had reduced glycolysis at rest,while CD8+ T cells also had reduced glycolysis following activation. ME/CFS patients had significant correlations between measures of T cell metabolism and plasma cytokine abundance that differed from healthy control subjects. Our data indicate that patients have impaired T cell metabolism consistent with ongoing immune alterations in ME/CFS that may illuminate the mechanism behind this disease.
更多信息
| 物种 | 人 |
|---|---|
| Contains | • Anti-human CD3 monospecific antibody complex • Anti-human CD28 monospecific antibody complex • Anti-human CD2 monospecific antibody complex |
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