Immune function studies macrophages

Holt, P.G. and Schon-Hegrad, M.A. (1987). Localization of T cells, macrophages and dendritic cells in rat respiratory tract tissue implications for immune function studies. 

In contrast to adaptive immune function, fewer studies have examined effects of TCDD on the innate immune system. Furthermore, of the limited data available, much of it is inconsistent. For example, natural killer (NK) cell activity has been reported to be unaffected,80,93 diminished,94 and increased95 following exposure to TCDD. Although a thorough assessment of AhR expression in all innate cell lineages has not been conducted, neutrophils and macrophages express the AhR,8,96 and neutrophils are affected... 

The effects of marijuana on immune function have been reviewed (122). The studies suggest that marijuana affects immune cell function of T and B lymphocytes, natural killer cells, and macrophages. In addition, cannabis appears to modulate host resistance, especially the secondary immune response to various infectious agents, both viral and bacterial. Lastly, marijuana may also affect the cytokine network, influencing the production and function of acute-phase and immune cytokines and modulating network cells, such as macrophages and T helper cells. Under some conditions, marijuana may be immunomodulatory and promote disease. 

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). 

A number of chemicals with demonstrable suppression of immune function produce this action via indirect effects. By and large, the approach that has been most frequently used to support an indirect mechanism of action is to show immune suppression after in vivo exposure but no immune suppression after in vitro exposure to relevant concentrations. One of the most often cited mechanisms for an indirect action is centered around the limited metabolic capabilities of immunocompetent cells and tissues. A number of chemicals have caused immune suppression when administered to animals but were essentially devoid of any potency when added directly to suspensions of lymphocytes and macrophages. Many of these chemicals are capable of being metabolized to reactive metabolites, including dime-thylnitrosamine, aflatoxin Bi, and carbon tetrachloride. Interestingly, a similar profile of activity (i.e., suppression after in vivo exposure but no activity after in vitro exposure) has been demonstrated with the potent immunosuppressive drug cyclophosphamide. With the exception of the PAHs, few chemicals have been demonstrated to be metabolized when added directly to immunocompetent cells in culture. A primary role for a reactive intermediate in the immune suppression by dimethylnitrosamine, aflatoxin Bi, carbon tetrachloride, and cyclophosphamide has been confirmed in studies in which these xenobiotics were incubated with suspensions of immunocompetent cells in the presence of metabolic activation systems (MASs). Examples of MASs include primary hepatocytes, liver microsomes, and liver homogenates. In most cases, confirmation of a primary role for a reactive metabolite has been provided by in vivo studies in which the metabolic capability was either enhanced or suppressed by the administration of an enzyme inducer or a metabolic inhibitor, respectively. 

Delta-9-THC is the main active constituent extracted from Cannabis sativa (Tuner, 1985 in Marijuana 1984, Ed. Harvey, DY, IRL Press, Oxford). Numerous articles have described not only psychotropic effects of cannabinoids but also their influence on the immune function [Hollister L. E., J. Psychoact. Drugs 24 (1992) 159-164]. The majority of in vitro studies have shown that cannabinoids have immunosuppressant effects inhibition of the mitogen induced proliferative responses of T lymphocytes and B lymphocytes [Luo, Y. D. et ah, Int. J. Immuno-pharmacol. (1992) 14,49-56 Schwartz, H. et at., J. Neuroimmunol. (1994) 55,107-115], inhibition of the activity of cytotoxic T cells [Klein et at., J. Toxicol. Environ. Health (1991) 32, 465-477], inhibition of the microbicidal activity of macrophages and of TNF-a synthesis [Arata, S. et at.. Life Sci. (1991) 49, 473-479 Fisher-Stenger et al., J. Pharm. Exp. Then (1993) 267, 1558-1565] and inhibition of the cytolytic activity and the TNFa production of large granular lymphoc3rtes [Kusher et al.. Cell. Immun. (1994) 154, 99-108],... 

The majority of literature published about Echinacea focuses on its activity as an immunostimulant. Many of the studies focus on the activity of macrophages and Echinacea s ability to activate and stimulate immune function. 

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