EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #15021_C
通过免疫密度分离法分选未被标记的T细胞
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总览
RosetteSep™人T细胞富集抗体混合物通过负选从全血分离T细胞。四聚体抗体复合物可识别非T细胞和红细胞（RBC）表面的糖蛋白A，从而靶向去除非目的细胞。使用 密度梯度离心液（如RosetteSep™ DM-L（产品号 #15705）或Lymphoprep™（产品号 #18060）离心后，非目的细胞会与红细胞一起沉淀。纯化的T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。
分类
细胞分选试剂盒
细胞类型
T 细胞
种属
人
样本来源
白膜层、全血
分选方法
负选
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 (9)
常见问题 (9)
文献 (61)
A deep single cell mass cytometry approach to capture canonical and noncanonical cell cycle states
Nature Communications 2025 Oct
Abstract
The cell cycle (CC) underpins diverse cell processes like cell differentiation, cell expansion, and tumorigenesis but current single-cell (sc) strategies study CC as: coarse phases, rely on transcriptomic signatures, use imaging modalities limited to adherent cells, or lack high-throughput multiplexing. To solve this, we develop an expanded, Mass Cytometry (MC) approach with 48 CC-related molecules that deeply phenotypes the diversity of scCC states. Using Cytometry by Time of Flight, we quantify scCC states across suspension and adherent cell lines, and stimulated primary human T cells. Our approach captures the diversity of scCC states, including atypical CC states beyond canonical definitions. Pharmacologically-induced CC arrest reveals that perturbations exacerbate noncanonical states and induce previously unobserved states. Notably, primary cells escaping CC inhibition demonstrated aberrant CC states compared to untreated cells. Our approach enables deeper phenotyping of CC biology that generalizes to diverse cell systems with simultaneous multiplexing and integration with MC platforms. Subject terms: Assay systems, Proteomics, Cell biology, Immunology, Systems biology
Retinol Binding Protein 4 reactivates latent HIV-1 by triggering canonical NF-κB, JAK/STAT5 and JNK signalling
Signal Transduction and Targeted Therapy 2025 Oct
Abstract
Reactivation of the latent viral reservoirs is crucial for a cure of HIV/AIDS. However, current latency reversing agents are inefficient, and the endogenous factors that have the potential to reactivate HIV in vivo remain poorly understood. To identify natural activators of latent HIV-1, we screened a comprehensive peptide/protein library derived from human hemofiltrate, representing the entire blood peptidome, using J-Lat cell lines harboring transcriptionally silent HIV-1 GFP reporter viruses. Fractions potently reactivating HIV-1 from latency contained human Retinol Binding Protein 4 (RBP4), the carrier of retinol (Vitamin A). We found that retinol-bound holo-RBP4 but not retinol-free apo-RBP4 strongly reactivates HIV-1 in a variety of latently infected T cell lines. Functional analyses indicate that this reactivation involves activation of the canonical NF-κB pathway and is strengthened by JAK/STAT5 and JNK signalling but does not require retinoic acid production. High levels of RBP4 were detected in plasma from both healthy individuals and people living with HIV-1. Physiological concentrations of RBP4 induced significant viral reactivation in latently infected cells from individuals on long-term antiretroviral therapy with undetectable viral loads. As a potent natural HIV-1 latency-reversing agent, RBP4 offers a novel approach to activating the latent reservoirs and bringing us closer to a cure. Subject terms: Preclinical research, Infectious diseases
A hexamerization-enhanced, Fc-silenced agonistic CD27 antibody amplifies T-cell effector functions as single agent and in combination with PD-1 blockade
Scientific Reports 2025 Jul
Abstract
HexaBody-CD27 (GEN1053/BNT313) is an investigational novel agonistic CD27 antibody engineered to enhance T-cell costimulation and promote antitumor immunity. Through the introduction of a hexamerization-enhancing mutation in the IgG Fc domain, HexaBody-CD27 was designed to drive clustering and activation of CD27 via intermolecular Fc:Fc interactions between membrane-bound antibodies, independent of crosslinking by FcγR-bearing cells. HexaBody-CD27 carries an Fc-silencing mutation to prevent T-cell depletion through Fc-mediated effector functions. In vitro, HexaBody-CD27 induced CD27 receptor signaling independent of FcγR-mediated crosslinking in a reporter assay. It also enhanced T-cell proliferation, cytotoxic activity and proinflammatory cytokine secretion in primary human lymphocytes. In contrast to benchmark IgG1 CD27 antibodies, HexaBody-CD27 did not induce phagocytosis of T cells in vitro. HexaBody-CD27 promoted ex vivo tumor infiltrating lymphocyte (TIL) expansion in non-small cell lung cancer (NSCLC) specimens, in particular of CD8 + TILs. The combination of HexaBody-CD27 with an anti-PD-1 antibody enhanced T-cell proliferation, cytokine secretion, and cytotoxic activity in vitro compared to either compound alone. In conclusion, HexaBody-CD27 enhanced T-cell activation and effector functions in an FcγR-crosslinking-independent manner, without inducing T-cell depletion. The immune agonist activity of HexaBody-CD27 was potentiated in combination with PD-1 blockade.
更多信息
| 物种 | 人类 |
|---|---|
| 样本来源 | 全血, 白膜层 |
| Selection Method | Negative |
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标记抗体
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抗人CD3抗体，clone UCHT1小鼠（BALB/c）Monoclonal IgG1抗体，抗人、黑猩猩CD3
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