Antibody-dependent cellular toxicity

Sheeja K, Kuttan G. (2007) Modulation of natural killer activity, antibody dependent cellular toxicity, and antibody dependent complement mediated cytotoxicity by andrographolide in normal and Ehrlich ascites carcinoma bearing mice. Integr Cancer Ther 6 66-73. 

Shields RL, Lai J, Keck R et al. Lack of fucose on human IgGlN-linked oligosaccharide improves binding to human Fcgamma RIII and antibody-dependent cellular toxicity. J Biol Chem 2002 277 26733-26740. 

The effect of echinacea on the immune system is controversial. In vivo human studies using commercially marketed formulations of E purpurea have shown increased phagocytosis, total circulating white blood cells, monocytes, neutrophils, and natural killer cells but not immunostimulation. In vitro, Epurpurea juice increased production of interleukins-1, -6, and -10, and tumor necrosis factor- by human macrophages. Enhanced natural killer cell activity and antibody-dependent cellular toxicity was also observed with E purpurea extract in cell lines from both healthy and immunocompromised patients. Studies using the isolated purified polysaccharides from Epurpurea have also shown cytokine activation. Polysaccharides by themselves, however, are unlikely to accurately reproduce the activity of the entire extract. 

G-CSF activates neutrophils, transforming them into cells capable of respiratory burst and release of secretory granules. It also modulates the expression of adhesion molecules on neutrophils as well as CD1 lb/CD18 and plasma elastase antigen levels. G-CSF induces proliferation of endothelial cells, phagocytic activity of neutrophils, reactive oxygen intermediate production by neutrophils and antibody-dependent cellular toxicity by neutrophils. 

There is a growing body of evidence suggesting that oc2-Macroglobulin plays an important role in human immune function. Specifically, studies have shown that the fast form can inhibit antibody-dependent cellular toxicity and natural killer (NK) cell-mediated cytolysis (49), as well as superoxide production by activated macrophages (50). 

Auranofin is a triethylphosphine gold derivative for oral administration. It is in some respects strikingly different from the rest. Some 25% of an oral dose is absorbed through the intestinal wall and blood concentrations are some 15-25% of those reached with parenteral therapy. Auranofin is bound to cellular elements of the blood, is excreted mainly in the feces, and exhibits less tissue retention and total body gold accumulation than parenteral forms. It is more effective in acute inflammatory models and is a potent inhibitor of lysosomal enzyme release, antibody-dependent cellular toxicity, and superoxide production. Auranofin also affects humoral and cellular immune reactions. However, some have found auranofin to be rather less effective than parenteral gold. Auranofin is used in doses of 2-9 mg/day (generally 6 mg/day), which is less than the dose originally recommended. 

IL-13 is a recently described cytokine secreted by different human T cell subsets and is a potent modulator of human monocyte and B cell function (Minty et al., 1993). Both CDT" and CDB" T cell clones synthesize IL-13 in response to antigen-specific or polyclonal stimuli (Zurawski and De Vries, 1994). IL-13 has profound effects on human monocyte morphology, surface antigen expression, antibody-dependent cellular toxicity and cytokine synthesis (Minty et al., 1993 McKenzie et al., 1993). In human monocytes stimulated by LPS, the production of proinflammatory cytokines, chemokines... 

Liver injury can be a result of both direct cytotoxicity and antibody-dependent cellular toxicity. Alcoholic liver disease is another example of possible immune-mediated damage. Acetaldehyde, produced by the metabolism of ethanol, forms adducts with hepatic proteins similar to halothane, resulting in higher antibody titers, to which some of the liver damage following ethanol ingestion may be attributed (Ramaiah et al., 2004). However,... 

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