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Since NNAV increased the Th1 and Th2 subsets differentiation (Figure 2(c)), we next explored whether Th17 cells were involved in the inhibitory effects on CD4 T-cell.
NNAV Partly Restored Dexamethasone-Induced Immunodepression.
The effects of NNAV on serum immunoglobulin in immune suppressed mice were determined by measuring the two major components, IgG and IgM concentrations.
The present study conducted the first in vivo evaluation of NNAV on three major components of the immune response.
Thus, in our study, the NNAV-induced enhancement of NK cell activity (Figure 1(a)) may be attributed to the direct or indirect effect of the stimulatory effect of NNAV on IFN-[gamma] production (Figure 2(a)).
In the present study, the administration of NNAV improved the anti-SRBC antibody production (Figure 1(b)), reflecting the augmentation of humoral response to SRBC.
We found that mitogen ConA-induced T cell proliferation was significantly suppressed by NNAV (Figure 3(a)).
It is interesting to know that NNAV produced an enhancing effect on innate and humoral immune responses partly due to its stimulatory effects on IFN-[gamma] and IL-4 production by Th1 and Th2 cells (Figure 2).
Similar regulatory effects of NNAV were obtained in DEX-induced immunosuppressed mice.
Our current research indicates that NNAV could selectively inhibit CD4 Th17 and CD8 T cells.
In this study, the dose effect relationship of NNAV varied significantly.
The present study documented that NNAV could strengthen the innate and humoral immune responses through the augmentation of NK and B cell function, or indirectly through the improvement on Th1 and Th2 cytokines secretion.
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- Nnamdi Azikiwe
- Nnamdi Azikiwe
- Nnamdi Azikiwe University
- Nnamdi Azikiwe University Teaching Hospital