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EasySep™ Mouse Memory CD4+ T Cell Isolation Kit

27.5-Minute cell isolation kit using immunomagnetic negative selection

概要

技术资料

数据及文献

概要

The EasySep™ Mouse Memory CD4+ T Cell Isolation Kit is designed to isolate pan-memory CD4+ T cells from single-cell suspensions of splenocytes or other tissues by negative selection. Unwanted cells are targeted for removal with biotinylated antibodies directed against non-memory CD4+ T cells (CD8, CD11b, CD11c, CD19, CD24, CD45R, CD45RB, CD49b, CD105 and TCRγ/δ) and streptavidin-coated magnetic particles (RapidSpheres™ ). Labeled cells are separated using an EasySep™ magnet without the use of columns. Desired cells are poured off into a new tube.

Learn more about our next-generation EasySep™ mouse cell isolation kits, featuring RapidSphere™ technology.

技术资料

Document Type	产品名称	Catalog #	Lot #	语言
Product Information Sheet	EasySep™ Mouse Memory CD4+ T Cell Isolation Kit	19767	All	English
Product Information Sheet	RoboSep™ Mouse Memory CD4+ T Cell Isolation Kit	19767RF	All	English
Safety Data Sheet 1	EasySep™ Mouse Memory CD4+ T Cell Isolation Kit	19767	All	English
Safety Data Sheet 2	EasySep™ Mouse Memory CD4+ T Cell Isolation Kit	19767	All	English
Safety Data Sheet 3	EasySep™ Mouse Memory CD4+ T Cell Isolation Kit	19767	All	English
Safety Data Sheet 1	RoboSep™ Mouse Memory CD4+ T Cell Isolation Kit	19767RF	All	English
Safety Data Sheet 2	RoboSep™ Mouse Memory CD4+ T Cell Isolation Kit	19767RF	All	English
Safety Data Sheet 3	RoboSep™ Mouse Memory CD4+ T Cell Isolation Kit	19767RF	All	English

数据及文献

Data

Figure 1. Typical EasySet™ Mouse Memory CD4+ T Cell Isolation Profile

Starting with mouse splenocytes, the memory CD4+ T cell (CD4+CD62L high CD44 high/int central memory and CD4+CD62L-CD44 high/int effector memory) content of the isolated fraction typically ranges from 78 - 96%. In the example above, the final purities of the start and isolated fractions are 5.3% and 90.2%, respectively.

Publications (1)

Nature communications 2020 T cell-intrinsic role for Nod2 in protection against Th17-mediated uveitis. R. J. Napier et al.

Abstract

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Abstract

Mutations in nucleotide-binding oligomerization domain-containing protein 2 (NOD2) cause Blau syndrome, an inflammatory disorder characterized by uveitis. The antimicrobial functions of Nod2 are well-established, yet the cellular mechanisms by which dysregulated Nod2 causes uveitis remain unknown. Here, we report a non-conventional, T cell-intrinsic function for Nod2 in suppression of Th17 immunity and experimental uveitis. Reconstitution of lymphopenic hosts with Nod2-/- CD4+ T cells or retina-specific autoreactive CD4+ T cells lacking Nod2 reveals a T cell-autonomous, Rip2-independent mechanism for Nod2 in uveitis. In naive animals, Nod2 operates downstream of TCR ligation to suppress activation of memory CD4+ T cells that associate with an autoreactive-like profile involving IL-17 and Ccr7. Interestingly, CD4+ T cells from two Blau syndrome patients show elevated IL-17 and increased CCR7. Our data define Nod2 as a T cell-intrinsic rheostat of Th17 immunity, and open new avenues for T cell-based therapies for Nod2-associated disorders such as Blau syndrome.

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