The EasySep™ Mouse FITC Positive Selection Kit II is designed to isolate mouse cells that are labeled with FITC-conjugated antibodies. Desired cells are targeted with antibody complexes recognizing FITC and dextran-coated magnetic particles. Labeled cells are separated using an EasySep™ magnet without the use of columns. Cells of interest remain in the tube while unwanted cells are poured off.
This product replaces the EasySep™ Mouse FITC Positive Selection Kit (Catalog #18555).
Cell Type B Cells, Dendritic Cells, Granulocytes and Subsets, Hematopoietic Stem and Progenitor Cells, Macrophages, Marrow Stromal Cells, Mesenchymal Stem and Progenitor Cells, Monocytes, Mononuclear Cells, Myeloid Cells, NK Cells, Other, Plasma, T Cells
Species Mouse
Sample Source Bone Marrow, Other, Spleen
Selection Method Positive
Application Cell Isolation
Brand EasySep, RoboSep
Area of Interest Immunology
Data Figures
Starting with mouse splenocytes, the purities of the start and final isolated fractions in the above example are 24.3% and 95.3%, respectively, using a FITCconjugated anti-mouse CD4 antibody and EasySep™ Mouse FITC Positive Selection Kit II.
Accumulation of ?? T cells in visceral fat with aging promotes chronic inflammation. M. E. C. Bruno et al. GeroScience 2022 jun
Abstract
Adipose tissue dysfunction is strongly linked to the development of chronic inflammation and cardiometabolic disorders in aging. While much attention has been given to the role of resident adipose tissue immune cells in the disruption of homeostasis in obesity, age-specific effects remain understudied. Here, we identified and characterized a population of ?? T cells, which show unique age-dependent accumulation in the visceral adipose tissue (VAT) of both mice and humans. Diet-induced obesity likewise increased ?? T cell numbers; however, the effect was greater in the aged where the increase was independent of fat mass. ?? T cells in VAT express a tissue-resident memory T cell phenotype (CD44hiCD62LlowCD69+) and are predominantly IL-17A-producing cells. Transcriptome analyses of immunomagnetically purified ?? T cells identified significant age-associated differences in expression of genes related to inflammation, immune cell composition, and adipocyte differentiation, suggesting age-dependent qualitative changes in addition to the quantitative increase. Genetic deficiency of ?? T cells in old age improved the metabolic phenotype, characterized by increased respiratory exchange ratio, and lowered levels of IL-6 both systemically and locally in VAT. Decreased IL-6 was predominantly due to reduced production by non-immune stromal cells, primarily preadipocytes, and adipose-derived stem cells. Collectively, these findings suggest that an age-dependent increase of tissue-resident ?? T cells in VAT contributes to local and systemic chronic inflammation and metabolic dysfunction in aging.
Combinatorial depletions of G-protein coupled receptor kinases in immune cells identify pleiotropic and cell type-specific functions. K. M. Glaser et al. Frontiers in immunology 2022
Abstract
G-protein coupled receptor kinases (GRKs) participate in the regulation of chemokine receptors by mediating receptor desensitization. They can be recruited to agonist-activated G-protein coupled receptors (GPCRs) and phosphorylate their intracellular parts, which eventually blocks signal propagation and often induces receptor internalization. However, there is growing evidence that GRKs can also control cellular functions beyond GPCR regulation. Immune cells commonly express two to four members of the GRK family (GRK2, GRK3, GRK5, GRK6) simultaneously, but we have very limited knowledge about their interplay in primary immune cells. In particular, we are missing comprehensive studies comparing the role of this GRK interplay for (a) multiple GPCRs within one leukocyte type, and (b) one specific GPCR between several immune cell subsets. To address this issue, we generated mouse models of single, combinatorial and complete GRK knockouts in four primary immune cell types (neutrophils, T cells, B cells and dendritic cells) and systematically addressed the functional consequences on GPCR-controlled cell migration and tissue localization. Our study shows that combinatorial depletions of GRKs have pleiotropic and cell-type specific effects in leukocytes, many of which could not be predicted. Neutrophils lacking all four GRK family members show increased chemotactic migration responses to a wide range of GPCR ligands, whereas combinatorial GRK depletions in other immune cell types lead to pro- and anti-migratory responses. Combined depletion of GRK2 and GRK6 in T cells and B cells shows distinct functional outcomes for (a) one GPCR type in different cell types, and (b) different GPCRs in one cell type. These GPCR-type and cell-type specific effects reflect in altered lymphocyte chemotaxis in vitro and localization in vivo. Lastly, we provide evidence that complete GRK deficiency impairs dendritic cell homeostasis, which unexpectedly results from defective dendritic cell differentiation and maturation in vitro and in vivo. Together, our findings demonstrate the complexity of GRK functions in immune cells, which go beyond GPCR desensitization in specific leukocyte types. Furthermore, they highlight the need for studying GRK functions in primary immune cells to address their specific roles in each leukocyte subset.
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Legal Statement: Users of this kit should ensure that they are entitled to use the antibody of interest. STEMCELL Technologies Inc. is not responsible for patent infringements or violations that may occur when using this product. 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 STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE.
