Goyarts, E., Bender, A.M., Matsui, M., Mammone, T., Maes, D. Estee Lauder Research Laboratories, Melville, NY and Dept. of Dermatology, Weill Medical College of Cornell University.

This study by researchers at Estee Lauder Research Laboratories and Cornell’s Weill Medical College demonstrated that norepinephrine binding to beta adrenergic receptors expressed on the surface of human Langerhans Cells (MatTek’s Human Dendritic Cells) mediated the decrease in immune function by preventing the activation of these immune cells. Psychological stress is potentially harmful to the skin because the nervous system responds by releasing norepinephrine, which may suppress cellular immunity by reducing the ability of Langerhans cells (LCs) to be activated. Published results on murine dendritic cells indicate a short exposure of norepinephrine in the presence of lipopolysaccharides (LPS) alters cytokine release and reduces T cell stimulation. Researchers at Estee Lauder Research Laboratories and the Dept. of Dermatology at Cornell’s Weill Medical College investigated the effect of norepinephrine on human LC activation. LC activation was evaluated by the release of LPS-inducible cytokines as well as the activation of T cells. Human bone marrow-derived LCs (MatTek Corp.), containing 40% plasmacytoid dendritic cells, were stimulated by LPS in the presence of norepinephrine. LCs were given a short-term (3h) exposure of norepinephrine at the beginning of the LPS treatment. The LPS-inducible markers, TNF-alpha and IL-12 p40, were down-regulated in the presence of norepinephrine. The LPS-inducible marker, IL-10, was not affected. The specificity of the response was evaluated with alpha and beta adrenergic receptor antagonists. The beta adrenergic receptor antagonists, propranolol and ICI-118,551, increased the LPS-inducible markers, TNF-alpha and IL-12 p40, in the presence of norepinephrine and LPS. The alpha adrenergic receptor antagonist, yohimbine, had no affect. Beta adrenergic receptors expressed on the surface of human LC mediate the decrease in immune function. A beta adrenergic receptor antagonist is likely to reverse stress-induced immunosuppression by directly inhibiting norepinephrine engagement of the beta adrenergic receptor.


Catecholamines, Cutaneous immune system, Cutaneous nerves, Cytokine release, DC-100-MM, Dendritic Cells (DC), IL-1b, Langerhan Cells (LC), Lipopolysaccharides (LPS, Nervous system, Norepinephrine, TNF-a

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