ImmunoCult™ 人CD3/CD28/CD2 T细胞激活剂

人T细胞激活扩增试剂

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产品号 #（选择产品）

产品号 #10970_C

人T细胞激活扩增试剂

产品优势

无需使用磁珠、饲养细胞或抗原，即可高效地激活和扩增人T细胞
提供温和的激活刺激，维持激活和扩增后T细胞的高活性
高度稳定，过滤灭菌的可溶性试剂

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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。

Data Figures

Figure 1. Activated Morphology of Human T Cells Stimulated With ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator

Image of human T cells isolated using the EasySep™ Human T Cell Isolation Kit (Catalog #17951), stimulated with ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator, and cultured in ImmunoCult™-XF T Cell Expansion Medium (Catalog #10981).

Figure 2. Activation of EasySep™ Isolated Human T Cells Stimulated With ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator

EasySep™-isolated human T cells were stimulated with ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator and cultured in ImmunoCult™-XF T Cell Expansion Medium. Activation of viable CD3+ T cells was assessed by CD25 expression using flow cytometry. On day 0, the frequency of CD25 positive cells was (A) 5.6 ± 2.4% (mean ± SD). Following 3 days of culture, the frequency of CD25 positive cells was (B) 88.8 ± 3.2% (mean ± SD) when stimulated with ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator.

Figure 3. Robust Human T Cell Expansion with ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator

EasySep™-isolated human T cells were expanded over 12 days with ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator in ImmunoCult™-XF T Cell Expansion Medium supplemented with Human Recombinant IL-2. On day 0, 1 x 10^6 EasySep™-isolated human T cells were stimulated with 25 μL of ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator in ImmunoCult™-XF T Cell Expansion Medium supplemented with 10 ng/mL Human Recombinant IL-2. On days 3, 5, 7, and 10, viable cells were counted and fresh medium supplemented with IL-2 was added. No additional ImmunoCult™ Human CD3/CD28/CD2 T Cell Activator was added during the 12-day culture period (mean ± SD in 6 experiments with 3 donors).

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Publications (5)

Plasma Gelsolin Inhibits CD8+ T-cell Function and Regulates Glutathione Production to Confer Chemoresistance in Ovarian Cancer. M. Asare-Werehene et al. 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.

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Competition between PAF1 and MLL1/COMPASS confers the opposing function of LEDGF/p75 in HIV latency and proviral reactivation. R. Gao et al. 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.

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PD-1+ melanocortin receptor dependent-Treg cells prevent autoimmune disease. F. Muhammad et al. 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.

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Species	Human
Contains	• Anti-human CD3 monospecific antibody complex • Anti-human CD28 monospecific antibody complex • Anti-human CD2 monospecific antibody complex