EasySep? Direct Human T Cell Isolation Kit
Immunomagnetic negative selection of untouched human T cells directly from whole blood
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Products for Your Protocol
To see all required products for your protocol, please consult the
Protocols and Documentation.
- EasySep? Magnet
Magnet for column-free immunomagnetic separation
- D-PBS (Without Ca++ and Mg++)
Dulbecco’s phosphate-buffered saline without calcium and magnesium
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Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (17)
Frequently Asked Questions
Publications (5)
Novel sACE2-Anti-CD16VHH Fusion Protein Surreptitiously Inhibits SARS-CoV-2 Variant Spike Proteins and Macrophage Cytokines, and Activates Natural Killer Cell Cytotoxicity
Vaccines 2025 Feb
Abstract
Background/Objectives: The SARS-CoV-2’s high mutations and replication rates contribute to its high infectivity and resistance to current vaccinations and treatments. The primary cause of resistance to most current treatments aligns within the coding regions for the spike S protein of SARS-CoV-2 that has mutated. As a potential novel immunotherapy, we generated a novel fusion protein composed of a soluble ACE2 (sACE2) linked to llama-derived anti-CD16 that targets different variants of spike proteins and enhances natural killer cells to target infected cells. Methods: Here, we generated a novel sACE2-AntiCD16VHH fusion protein using a Gly4Ser linker, synthesized and cloned into the pLVX-EF1alpha-IRES-Puro vector, and further expressed in ExpiCHO-S cells and purified using Ni+NTA chromatography. Results: The fusion protein significantly blocked SARS-CoV-2 alpha, beta, delta, gamma, and omicron S-proteins binding and activating angiotensin-converting enzyme receptor-2 (ACE2) on ACE2-expressing RAW-Blue macrophage cells and the secretion of several key inflammatory cytokines, G-CSF, MIP-1A, and MCP-1, implicated in the cytokine release storm (CRS). The sACE2-Anti-CD16VHH fusion protein also bridged NK cells to ACE2-expressing human lung carcinoma A549 cells and significantly activated NK-dependent cytotoxicity. Conclusions: The findings show that a VHH directed against CD16 could be an excellent candidate to be linked to soluble ACE2 to generate a bi-specific molecule (sACE2-AntiCD16VHH) suitable for bridging effector cells and infected target cells to inhibit SARS-CoV-2 variant spike proteins binding to the ACE2 receptor in the RAW-Blue cell line and pro-inflammatory cytokines and to activate natural killer cell cytotoxicity.
PD-L1+ neutrophils mediate immune regulation of CD8+ T cells in halo nevi
Frontiers in Immunology 2025 Aug
Abstract
BackgroundHalo nevi are clinically common and are characterized by a circle of leukoderma around the central melanocytic nevus. Studies have shown that the pathogenesis of halo nevi is similar to that of vitiligo and is associated with the role of CD8? T lymphocytes in melanocyte destruction. Histopathological findings have revealed neutrophil infiltration in halo nevi; however, the specific immune mechanisms involving neutrophils have not been thoroughly investigated. In the present study, we investigated the role of neutrophils in halo nevi using histopathological and immunological analyses.MethodsTo this end, we examined the infiltration patterns of immune cells in halo nevi, with a particular focus on IFN-γ-induced PD-L1 expression in neutrophils and its potential immunoregulatory effects.ResultsThe results demonstrated that IFN-γ expression in the lesional skin of halo nevi contributed to the induction of PD-L1 expression in neutrophils. PD-L1? neutrophils promoted apoptosis and suppressed the function of CD8? T lymphocytes. Notably, some halo nevi showed a tendency to spontaneous regression, but the underlying mechanisms remain unclear, and this regulatory mechanism influences the local immune response and may facilitate the repigmentation of the surrounding leukoderma in halo nevi.ConclusionsThis study is the first to explore the involvement of neutrophils in halo nevi and reveal the potential immunoregulatory role of PD-L1 in this process. The elucidation of this mechanism not only provides a more comprehensive understanding of autoimmune skin diseases but may also offer new strategies for targeted therapy in other related disorders, such as vitiligo.
PD-1/CD80
Nature Communications 2024 May
Abstract
Only a minority of cancer patients benefit from immune checkpoint blockade therapy. Sophisticated cross-talk among different immune checkpoint pathways as well as interaction pattern of immune checkpoint molecules carried on circulating small extracellular vesicles (sEV) might contribute to the low response rate. Here we demonstrate that PD-1 and CD80 carried on immunocyte-derived sEVs (I-sEV) induce an adaptive redistribution of PD-L1 in tumour cells. The resulting decreased cell membrane PD-L1 expression and increased sEV PD-L1 secretion into the circulation contribute to systemic immunosuppression. PD-1/CD80+ I-sEVs also induce downregulation of adhesion- and antigen presentation-related molecules on tumour cells and impaired immune cell infiltration, thereby converting tumours to an immunologically cold phenotype. Moreover, synchronous analysis of multiple checkpoint molecules, including PD-1, CD80 and PD-L1, on circulating sEVs distinguishes clinical responders from those patients who poorly respond to anti-PD-1 treatment. Altogether, our study shows that sEVs carry multiple inhibitory immune checkpoints proteins, which form a potentially targetable adaptive loop to suppress antitumour immunity. Immune checkpoint inhibition is a successful form of immune therapy; however response rates vary widely among individual patients. Here authors show that circulating small extracellular vesicles might contribute to poor response to anti-PD-1 treatment by carrying PD-1 and CD80 which results in higher level of vesicular PD-L1 expression in the circulation at the expense of expression on tumour cell membranes, causing immunosuppression.
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PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT 海角破解版, REFER TO WWW.海角破解版.COM/COMPLIANCE.
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT 海角破解版, REFER TO WWW.海角破解版.COM/COMPLIANCE.
