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All phases of the AP response, from macrophage activation and stimulation of glucocorticoid secretion to AP protein expression appear to be under the control of similar molecular mechanisms to those during the turpentine\u2010induced AP response. The AP protein content in the circulation 24 h after either soman, paraoxon or turpentine administration was injury\u2010specific. Both soman and paraoxon poisoning were characterized by significantly increased synthesis of <jats:italic>\u03b1<\/jats:italic><jats:sub>1<\/jats:sub>\u2010acid glycoprotein (AGP) that displayed an immunomodulatory effect <jats:italic>in vitro<\/jats:italic>. This result suggests that after organophosphate poisoning AGP participates <jats:italic>in vivo<\/jats:italic> in a negative feedback mechanism that prevents over\u2010activity of the immune system. 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