By cell surface phenotyping we originally reported that atypical MBCs expressed FcRL4 (Weiss et al., 2009).
This analysis revealed the differential expression of several inhibitory receptors including ones that we previously determined were upregulated in atypical MBCs by cell surface phenotyping (Weiss et al., 2009).
The development and progression of breast tumours has been proposed to be driven by breast cancer stem cells (CSC) identified by the cell surface phenotype ESA+CD44+CD24low or aldehyde dehydrogenase (ALDH1) activity [ 7, 8].
The cells responsible for this effect, called IFN-gamma-stimulated monocyte-derived cells (IFNgamma-MdC), derive from mouse spleen, blood, and bone marrow monocytes and are distinguished from known macrophage populations by mode of generation, cell surface phenotype, and function.
The cells consisted of >90% mature myeloid DCs as determined by their morphology and their cell surface phenotype (i.e CD1a+, CD80+ and CD86+).
The TCR specificity of clones was validated by FACS using staining with mAbs specific for CD3, Vα24, Vβ11 and the invariant iNKT cell TCR chain (6B11), and the cell surface phenotype was determined by staining with CD4 and CD8α specific mAbs.
The number and cell surface phenotype of liver NKT cells recovered by perfusion and by the traditional method were comparable.
Peripheral blood mononuclear cells from healthy subjects were cultured in the presence or absence of different combinations of IL-17s and changes in relative numbers and cell surface phenotype of NK cells and CD56+CD3+ cells measured by flow cytometry.
Cell surface phenotype of CD133+ retinal cells and CD133- cells was assessed by multiparameter flow cytometry (FACS Calibur, BD biosciences).
Differentiation into nontumorigenic cells was evidenced by H&E and cytokeratin staining (criterion d), and cultured spheroid cells exhibited a distinctive cell surface phenotype, CD49f (criterion e).
