scholarly journals Differential Effects ofNaja naja atraVenom on Immune Activity

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Jian-Qun Kou ◽  
Rong Han ◽  
Yin-Li Xu ◽  
Xiao-Lan Ding ◽  
Shu-Zhi Wang ◽  
...  

Previous studies reported thatNaja naja atravenom (NNAV) inhibited inflammation and adjuvant arthritis. Here we investigated the role of NNAV in regulation of immune responses in mice. Oral administration of NNAV to normal mice showed significant increase in natural killer cell activity, B lymphocyte proliferation stimulated by lipopolysaccharides, and antibody production in response to sheep red blood cells. Meanwhile, NNAV markedly decreased T lymphocyte proliferation stimulated by concanavalin A, arrested the cell cycle at G0/G1phase, and suppressed CD4 and CD8 T cell divisions. Furthermore, NNAV inhibited the dinitrofluorobenzene-induced delayed-type hypersensitivity reaction. This modulation of immune responses may be partly attributed to the selective increase in Th1 and Th2 cytokines (IFN-γ, IL-4) secretion and inhibition of Th17 cytokine (IL-17) production. In dexamethasone-induced immunosuppressed mice, NNAV restored the concentration of serum IgG and IgM, while decreasing the percentage of CD4 and CD8 T-cell subsets. These results indicate that NNAV enhances the innate and humoral immune responses while inhibiting CD4 Th17 and CD8 T cell actions, suggesting that NNAV could be a potential therapeutic agent for autoimmune diseases.

1997 ◽  
Vol 84 (3_suppl) ◽  
pp. 1296-1298 ◽  
Author(s):  
Tsutomu Kamei ◽  
Hiroaki Kumano ◽  
Sumio Masumura

For 8 medical students influences of psychological stress or humor on T-cell subset percentages and natural killer cell activity were investigated by measuring these parameters before and after an examination and before and after watching a comedy video. Although T-cell subsets were not significantly affected by either stimulus and natural killer cell activity was not affected by the examination, the latter was significantly decreased after watching the comedy video.


1998 ◽  
Vol 275 (4) ◽  
pp. R1227-R1231
Author(s):  
H. B. Nielsen ◽  
N. H. Secher ◽  
M. Kappel ◽  
B. K. Pedersen

This study evaluated whether N-acetylcysteine (NAC) attenuates the reduced lymphocyte proliferation and natural killer (NK) cell activity responses to exercise in humans. Fourteen oarsmen were double-blind randomized to either NAC (6 g daily for 3 days) or placebo groups. During 6-min “all-out” ergometer rowing, the concentration of lymphocytes in the peripheral blood increased, with no significant difference between NAC and placebo as reflected in lymphocyte subsets: CD4+, CD8+, CD16+, and CD19+ cells. The phytohemagglutinin-stimulated lymphocyte proliferation decreased from 9,112 ± 2,865 to 5,851 ± 1,588 cpm ( P < 0.05), but it was not affected by NAC. During exercise, the NK cell activity was elevated from 17 ± 3 to 38 ± 4% and it decreased to 7 ± 1% below the resting value 2 h into recovery. Yet, when evaluated as lytic units per CD16+ cell, the NK cell activity decreased during and after exercise without a significant effect of NAC. We conclude that NAC does not attenuate the reduction in lymphocyte proliferation and NK cell activity associated with intense exercise.


1982 ◽  
Vol 155 (5) ◽  
pp. 1579-1584 ◽  
Author(s):  
U Landegren ◽  
U Ramstedt ◽  
I Axberg ◽  
M Ullberg ◽  
M Jondal ◽  
...  

Out of a panel of seven monoclonal antibodies with affinity for human lymphoid cells, three were shown to prevent cytotoxic T cell activity, whereas none affected natural killer cell activity when applied without complement. Anti-OKT3 and anti-Leu-2a, with affinity for all T cells and the cytotoxic/suppressive subset, respectively were both shown to inhibit T killing by their interaction with the effector cell. For anti-OKT3, the inhibition remained after free antibody was washed away. Anti-Leu-2a, in contrast, induced a rapidly reversible inhibition. Using a single cell assay, anti-OKT3 was shown to reduce the lytic ability without affecting target cell binding, whereas anti-Leu-2a prevented the effectors from binding target cells.


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