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Human Peripheral Blood CD4+ T Cells, Frozen

Primary human cells, frozen

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Human Peripheral Blood CD4+ T Cells, Frozen

Primary human cells, frozen

1.5 x 107 cells

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Catalog #70026
725 USD

Overview

Primary human CD4+ T cells were isolated from peripheral blood (PB) mononuclear cells (MNCs) using negative immunomagnetic separation techniques. PB was collected using either citrate-phosphate-dextrose (CPD) or acid-citrate-dextrose solution A (ACDA) as an anticoagulant.

Cells were obtained using Institutional Review Board (IRB) approved consent forms and protocols.

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Contains:
• CryoStor® CS10
Subtype:
Frozen
Cell Type:
T Cells; T Cells, CD4+
Species:
Human
Cell and Tissue Source:
Peripheral Blood
Donor Status:
Normal
Purity:
The purity of CD4+ T cells is ≥ 85% by flow cytometry.

Scientific Resources

Product Documentation

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Educational Materials

(2)

Product 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.

Data and Publications

Publications

(1)
Blood 2015 FEB

Evidence of an oncogenic role of aberrant TOX activation in cutaneous T-cell lymphoma.

Huang Y et al.

Abstract

TOX is a nuclear factor essential for the development of CD4(+) T cells in the thymus. It is normally expressed in low amounts in mature CD4(+) T cells of the skin and the peripheral blood. We have recently discovered that the transcript levels of TOX were significantly increased in mycosis fungoides, the most common type of cutaneous T-cell lymphoma (CTCL), as compared to normal skin or benign inflammatory dermatoses. However, its involvement in advanced CTCL and its biological effects on CTCL pathogenesis have not been explored. In this study, we demonstrate that TOX expression is also enhanced significantly in primary CD4(+)CD7(-) cells from patients with Sézary syndrome, a leukemic variant of CTCL, and that high TOX transcript levels correlate with increased disease-specific mortality. Stable knockdown of TOX in CTCL cells promoted apoptosis and reduced cell cycle progression, leading to less cell viability and colony-forming ability in vitro and to reduced tumor growth in vivo. Furthermore, TOX knockdown significantly increased 2 cyclin-dependent kinase (CDK) inhibitors, CDKN1B and CDKN1C. Lastly, blocking CDKN1B and CDKN1C reversed growth inhibition of TOX knockdown. Collectively, these findings provide strong evidence that aberrant TOX activation is a critical oncogenic event for CTCL.
STEMCELL TECHNOLOGIES INC.’S QUALITY MANAGEMENT SYSTEM IS CERTIFIED TO ISO 13485. PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.