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Norepinephrine modulates human dendritic cell activation by altering cytokine release
Author(s) -
Goyarts Earl,
Matsui Mary,
Mammone Tom,
Bender Anna M.,
Wagner John A.,
Maes Daniel,
Granstein Richard D.
Publication year - 2008
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2007.00677.x
Subject(s) - cytokine , microbiology and biotechnology , endocrinology , tumor necrosis factor alpha , receptor , population , forskolin , medicine , cord blood , dendritic cell , chemistry , biology , immunology , immune system , environmental health
Norepinephrine (NE) can modulate dendritic cell (DC) activation in animal models, but the response of human DC to NE and other response modifiers is as yet not completely understood. Here we report the effect of NE on the cytokine response of a mixed population of human DC cells to extracellular stimuli. These cells were obtained by differentiating human cord blood CD34+ precursor cells. NE inhibited the lipopolysaccharide (LPS)‐stimulated production of interleukin (IL)‐23, IL‐12 p40, tumor necrosis factor (TNF)‐alpha and IL‐6 whereas the expression of IL‐10 was not significantly affected. Thus, human cord blood‐derived DC respond to NE in a manner similar to mouse Langerhans cells (LC). Furthermore, forskolin also inhibited the LPS‐induced levels of TNF‐alpha, IL‐12 p40, IL‐23 p19 and IL‐6, supporting the hypothesis that the effects of NE are mediated by cAMP. Data from experiments using inhibitors of adrenergic receptors suggest that NE acts through beta‐adrenergic receptors. As IL‐23 promotes the differentiation of CD4+ T cells required for T H 1‐mediated immunity, we suggest that NE decreases the differentiation of CD4+ T cells needed for T H 1‐mediated contact hypersensitivity and that NE is a candidate regulator of human DC functions in the skin.