11/2/2022 0 Comments Nod scid mousePhenotypic and functional characterization of natural killer cells in rheumatoid arthritis-regulation with interleukin-15. NK cell subsets in idiopathic recurrent miscarriage and renal transplant patients. Exploring the NK cell platform for cancer immunotherapy. Why natural killer cells in triple negative breast cancer? World Journal of Clinical Oncology. Values of ∗∗ P < 0.01 were considered statistically significant. FCM histograms show representative data of three independent experiments. (g) Statistical analysis of the FCM data for the IFN- γ expression on DX5 + populations of the splenocytes from poly(I:C)-treated mice. (f) Representative FCM data show the IFN- γ expression gated on DX5 + populations of the splenocytes from poly(I:C)-treated mice. (e) Statistical analysis of the FCM data for the IFN- γ expression on splenic DX5 + populations. (d) Representative FCM data show the IFN- γ expression gated on DX5 + populations of the splenocytes from naïve mice. (c) Statistical analysis of the ELISA data for IFN- γ in the culture supernatant. (b) Statistical analysis of the FCM data for IFN- γ and DX5 expression. (a) Representative FCM data show IFN- γ in and the expression of DX5 on the splenocytes from CB17/SCID and NOD/SCID mice. The splenocytes from naïve (a–e) or poly(I:C)-treated (f, g) mice were cultured with cytokines for 48 h. Caution should be taken when considering the use of NOD/SCID mice as an NK-deficient model.Īssay of IFN- γ in cells and cell culture supernatant in vitro. There was no significant difference in the proportion of splenic NK cells between CB17/SCID and NOD/SCID mice, and the function of NK cells was only partially compromised in NOD/SCID mice. After in vitro stimulation with cytokines, the splenocytes from CB17/SCID mice showed higher IFN- γ production than those from NOD/SCID mice however, NK cells did not. The splenocytes from CB17/SCID mice showed higher cytotoxicity than those from NOD/SCID mice, while the cytotoxicity of purified NK cells basically did not differ between the two strains. The scid mutation is in the DNA repair complex protein Prkdc and renders the mice B and T cell deficient. Moreover, the NKG2D and Ly49A levels in NK cells from NOD/SCID mice were higher than those from CB17/SCID. The mice carry two mutations on the NOD/ShiLtJ genetic background severe combined immune deficiency (scid) and a complete null allele of the IL2 receptor common gamma chain (IL2rgnull).The perforin levels in NK cells were similar between the poly(I:C)-treated CB17/SCID and NOD/SCID mice, while the granzyme B and NKG2A/C/E levels in NK cells from NOD/SCID mice were significantly lower than those from CB17/SCID mice. The proportion of splenic NK cells did not differ significantly between NOD/SCID and CB17/SCID mice. Splenocytes from naïve or poly(I:C)-treated mice were isolated for phenotyping and analysis of cytotoxicity-related molecules and inhibitory receptors for cytotoxicity assay, purified NK cells were also used. However, the actual status of NK cells in NOD/SCID mice and CB17/SCID mice in comparison with that in BALB/c mice has not been sufficiently evaluated. NOD/SCID mice have been used as a model of this type in research. Natural killer (NK) cell-deficient mice are useful models in biomedical research.
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