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
在无磁珠、饲养细胞或抗原的体系下，实现T细胞的稳定激活和扩增。
该产品温和的激活刺激效果可确保活化T细胞的高活性，并可在ImmunoCult™-XF T细胞扩增培养基（产品号 #10981）或其它用于培养人T细胞的培养基中进一步扩增。ImmunoCult™人CD3/CD28/CD2 T细胞激活剂由可溶性抗体复合物组成，可结合并交联细胞表面配体CD3、CD28和CD2，从而为T细胞激活提供所需的初级和共刺激信号。
本产品专为研究应用而设计。如果您需要适用于细胞治疗生产的试剂，ImmunoCult™人 CD3/CD28/CD2 T细胞激活剂（产品号 #100-0785）符合相关GMP要求。
该产品温和的激活刺激效果可确保活化T细胞的高活性，并可在ImmunoCult™-XF T细胞扩增培养基（产品号 #10981）或其它用于培养人T细胞的培养基中进一步扩增。ImmunoCult™人CD3/CD28/CD2 T细胞激活剂由可溶性抗体复合物组成，可结合并交联细胞表面配体CD3、CD28和CD2，从而为T细胞激活提供所需的初级和共刺激信号。
本产品专为研究应用而设计。如果您需要适用于细胞治疗生产的试剂，ImmunoCult™人 CD3/CD28/CD2 T细胞激活剂（产品号 #100-0785）符合相关GMP要求。
该产品温和的激活刺激效果可确保活化T细胞的高活性，并可在ImmunoCult™-XF T细胞扩增培养基（产品号 #10981）或其它用于培养人T细胞的培养基中进一步扩增。ImmunoCult™人CD3/CD28/CD2 T细胞激活剂由可溶性抗体复合物组成，可结合并交联细胞表面配体CD3、CD28和CD2，从而为T细胞激活提供所需的初级和共刺激信号。
本产品专为研究应用而设计。如果您需要适用于细胞治疗生产的试剂，ImmunoCult™人 CD3/CD28/CD2 T细胞激活剂（产品号 #100-0785）符合相关GMP要求。
该产品温和的激活刺激效果可确保活化T细胞的高活性，并可在ImmunoCult™-XF T细胞扩增培养基（产品号 #10981）或其它用于培养人T细胞的培养基中进一步扩增。ImmunoCult™人CD3/CD28/CD2 T细胞激活剂由可溶性抗体复合物组成，可结合并交联细胞表面配体CD3、CD28和CD2，从而为T细胞激活提供所需的初级和共刺激信号。
本产品专为研究应用而设计。如果您需要适用于细胞治疗生产的试剂，ImmunoCult™人 CD3/CD28/CD2 T细胞激活剂（产品号 #100-0785）符合相关GMP要求。
包含
• Anti-human CD3 monospecific antibody complex
• Anti-human CD28 monospecific antibody complex
• Anti-human CD2 monospecific antibody complex
亚型
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 (22)
文献 (5)
Plasma Gelsolin Inhibits CD8+ T-cell Function and Regulates Glutathione Production to Confer Chemoresistance in Ovarian Cancer. Cancer research 2020 sep
Abstract
Although initial treatment of ovarian cancer is successful, tumors typically relapse and become resistant to treatment. Because of poor infiltration of effector T cells, patients are mostly unresponsive to immunotherapy. Plasma gelsolin (pGSN) is transported by exosomes (small extracellular vesicle, sEV) and plays a key role in ovarian cancer chemoresistance, yet little is known about its role in immunosurveillance. Here, we report the immunomodulatory roles of sEV-pGSN in ovarian cancer chemoresistance. In chemosensitive conditions, secretion of sEV-pGSN was low, allowing for optimal CD8+ T-cell function. This resulted in increased T-cell secretion of IFN$\gamma$, which reduced intracellular glutathione (GSH) production and sensitized chemosensitive cells to cis-diaminedichloroplatinum (CDDP)-induced apoptosis. In chemoresistant conditions, increased secretion of sEV-pGSN by ovarian cancer cells induced apoptosis in CD8+ T cells. IFN$\gamma$ secretion was therefore reduced, resulting in high GSH production and resistance to CDDP-induced death in ovarian cancer cells. These findings support our hypothesis that sEV-pGSN attenuates immunosurveillance and regulates GSH biosynthesis, a phenomenon that contributes to chemoresistance in ovarian cancer. SIGNIFICANCE: These findings provide new insight into pGSN-mediated immune cell dysfunction in ovarian cancer chemoresistance and demonstrate how this dysfunction can be exploited to enhance immunotherapy.
Competition between PAF1 and MLL1/COMPASS confers the opposing function of LEDGF/p75 in HIV latency and proviral reactivation. Science advances 2020 may
Abstract
Transcriptional status determines the HIV replicative state in infected patients. However, the transcriptional mechanisms for proviral replication control remain unclear. In this study, we show that, apart from its function in HIV integration, LEDGF/p75 differentially regulates HIV transcription in latency and proviral reactivation. During latency, LEDGF/p75 suppresses proviral transcription via promoter-proximal pausing of RNA polymerase II (Pol II) by recruiting PAF1 complex to the provirus. Following latency reversal, MLL1 complex competitively displaces PAF1 from the provirus through casein kinase II (CKII)-dependent association with LEDGF/p75. Depleting or pharmacologically inhibiting CKII prevents PAF1 dissociation and abrogates the recruitment of both MLL1 and Super Elongation Complex (SEC) to the provirus, thereby impairing transcriptional reactivation for latency reversal. These findings, therefore, provide a mechanistic understanding of how LEDGF/p75 coordinates its distinct regulatory functions at different stages of the post-integrated HIV life cycles. Targeting these mechanisms may have a therapeutic potential to eradicate HIV infection.
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.
更多信息
| 种属 | Human |
|---|---|
| Contains | • Anti-human CD3 monospecific antibody complex • Anti-human CD28 monospecific antibody complex • Anti-human CD2 monospecific antibody complex |
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