Open AccessInhibition of natural killer (NK) cell activity against varicella‐zoster virus (VZV)‐infected fibroblasts and lymphocyte activation in response to VZV antigen by nitric oxide‐releasing agents
Author(s) -
ITO M.,
WATANABE M.,
KAMIYA H.,
SAKURAI M.
Publication year - 1996
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1996.d01-807.x
Subject(s) - varicella zoster virus , immunology , biology , antigen , cytotoxicity , cellular immunity , lymphocyte , interferon , t cell , natural killer cell , il 2 receptor , antibody dependent cell mediated cytotoxicity , immune system , virus , chemistry , antibody , in vitro , biochemistry , monoclonal antibody
The addition of nitric oxide (NO)‐releasing agents, S‐nitroso‐N‐acetyl‐DL‐penicillamine (SNAP), 1‐hydroxy‐2‐oxo‐2,3‐bis(2‐aminoethyl)‐1‐triazene (NOC18), 30{(±)‐(E)‐ethyl‐2′‐[(E)‐hydroxyimino]‐5‐nitro‐3‐hexenecarbamoyl}‐pyridine (NOR4) significantly inhibited NK cell activity against VZV‐infected cells, while antibody‐dependent cell‐mediated cytotoxicity (ADCC) against VZV‐infected cells was unaffected. Interferon‐alpha (IFN‐α) production by non‐adherent peripheral blood mononuclear cells (NPBMC) cultured with VZV‐infected cells was decreased by the addition of NO‐releasing agents. Lymphocyte proliferation and the expression IL‐2 receptor (CD25) in response to VZV antigen were also inhibited by the addition of NO‐releasing agents. These results suggest that the production of NO by an inflammatory process may lead to inhibition of NK cell‐ and T cell‐mediated immunity to VZV infection.