Natural killer (NK)-cell activity in sorted subsets of peripheral blood mononuclear cells from patients with severe combined immunodeficiency

1987 ◽  
Vol 7 (3) ◽  
pp. 198-202 ◽  
Author(s):  
R. J. M. Ten Berge ◽  
P. Th. A. Schellekens ◽  
A. Budding-Koppenol ◽  
L. J. Dooren ◽  
J. M. Vossen
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Nk Cell ◽  
Severe Combined Immunodeficiency ◽  
Cell Activity ◽  
Combined Immunodeficiency ◽  
Nk Cell Activity ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

scholarly journals Assessment of NK Cell Activity Based on NK Cell-Specific Receptor Synergy in Peripheral Blood Mononuclear Cells and Whole Blood

2020 ◽  
Vol 21 (21) ◽  
pp. 8112
Author(s):  
Jung Min Kim ◽  
Eunbi Yi ◽  
Hyungwoo Cho ◽  
Woo Seon Choi ◽  
Dae-Hyun Ko ◽  
...  
Keyword(s):  
Nk Cells ◽  
Peripheral Blood Mononuclear Cells ◽  
Whole Blood ◽  
Mononuclear Cells ◽  
Nk Cell ◽  
Cell Activity ◽  
Target Cells ◽  
Nk Cell Activity ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Natural killer (NK) cells are cytotoxic innate lymphocytes endowed with a unique ability to kill a broad spectrum of cancer and virus-infected cells. Given their key contribution to diverse diseases, the measurement of NK cell activity (NKA) has been used to estimate disease prognosis or the effect of therapeutic treatment. Currently, NKA assays are primarily based on cumbersome procedures related to careful labeling and handling of target cells and/or NK cells, and they require a rapid isolation of peripheral blood mononuclear cells (PBMCs) which often necessitates a large amount of blood. Here, we developed an ELISA-based whole blood (WB) NKA assay involving engineered target cells (P815-ULBP1+CD48) providing defined and synergistic stimulation for NK cells via NKG2D and 2B4. WB collected from healthy donors (HDs) and patients with multiple myeloma (MM) was stimulated with P815-ULBP1+CD48 cells combined with IL-2. Thereafter, it utilized the serum concentrations of granzyme B and IFN-γ originating in NK cells as independent and complementary indicators of NKA. This WB NKA assay demonstrated that MM patients exhibit a significantly lower NKA than HDs following stimulation with P815-ULBP1+CD48 cells and had a good correlation with the commonly used flow cytometry-based PBMC NKA assay. Moreover, the use of P815-ULBP1+CD48 cells in relation to assessing the levels of NKG2D and 2B4 receptors on NK cells facilitated the mechanistic study and led to the identification of TGF-β1 as a potential mediator of compromised NKA in MM. Thus, our proposed WB NKA assay facilitates the reliable measurement of NKA and holds promise for further development as both a clinical and research tool.

scholarly journals Non-Coated Rituximab Induces Highly Cytotoxic Natural Killer Cells From Peripheral Blood Mononuclear Cells via Autologous B Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Chao Niu ◽  
Yongchong Chen ◽  
Min Li ◽  
Shan Zhu ◽  
Lei Zhou ◽  
...  
Keyword(s):  
B Cells ◽  
Nk Cells ◽  
Natural Killer ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Nk Cell ◽  
New Method ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Natural killer (NK) cells are becoming valuable tools for cancer therapy because of their cytotoxicity against tumor cells without prior sensitization and their involvement in graft-versus-host disease; however, it is difficult to obtain highly cytotoxic NK cells without adding extra feeder cells. In this study, we developed a new method for obtaining highly cytotoxic NK cells from peripheral blood mononuclear cells (PBMCs) independently of extra feeder cell addition using rituximab not coated on a flask (non-coated rituximab). We found that rituximab could promote both the activation and expansion of NK cells from PBMCs, irrespective of being coated on a flask or not. However, NK cells activated by non-coated rituximab had much greater antitumor activity against cancer cells, and these effects were dependent on autologous living B cells. The antibody-dependent cellular cytotoxicity effect of NK cells activated by non-coated rituximab was also more substantial. Furthermore, these cells expressed higher levels of CD107a, perforin, granzyme B, and IFN-γ. However, there was no difference in the percentage, apoptosis, and cell-cycle progression of NK cells induced by coated and non-coated rituximab. Non-coated rituximab activated NK cells by increasing AKT phosphorylation, further enhancing the abundance of XBP1s. In conclusion, we developed a new method for amplifying NK cells with higher antitumor functions with non-coated rituximab via autologous B cells from PBMCs, and this method more efficiently stimulated NK cell activation than by using coated rituximab.

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