research interests have centred on the pivotal role that monocytes play in coordinating immune responses by releasing cytokines, prostaglandins and fatty acids. The cytokines released from monocytes, particularly interleukin-1 and tumour necrosis factor-alpha, can also amplify the antigen-induced activation of T-cells whereas prostaglandins such as PGE2 and fatty acids are potent inhibitors of activation. Recent data indicates that IL-1-stimulated fatty acid release can result in the biosynthesis of fatty acid ethanolamides including arachidonyl ethanolamide (anandamide) in addition to eicosanoids. Arachidonyl ethanolamide, regarded as an endogenous ligand for cannabinoid receptors, has been shown in our studies to modulate the activity of many monocyte and lymphocyte functions. Several major areas are being studied, including modulation of human monocyte and T-lymphocyte activities by PGE2, fatty acids and fatty acid ethanolamides.  Current work has been directed toward an attempt to understand the mechanisms by which PGE2 and fatty acids regulate: cytokine production, phagocytosis of E. coli O157 in human monocytes and the downregulation of human CD4+ lymphocyte function, especially  via the generation of intracellular cyclic AMP and cyclic GMP. The role of novel steroids, acting via PGs, on the modulation of immune cell activities is also being investigated as these provide another important potential therapeutic target

Negative feedback reguation of Immune responses by PGE2