Abstract
Considering the commonality of chronic stress in today’s society, and vital role of the immune system in overall health, it is important to understand the molecular mechanisms by which stress interferes with immune function. In vitro studies have shown one stress hormone, norepinephrine (NE), decreases functionality and proliferation of immune cells including thymus-derived lymphocytes (T cells). In response to a pathogen, T cells undergo a series of cell divisions to generate sufficient numbers of “effector” T cells; this is critical for a successful adaptive immune response. It is unclear how NE reduces the functionality of T cells and if NE impacts T cell subsets equally. Here, we examine the effect of NE on freshly isolated human CD8 T cell function in vitro (n = 16). We found memory CD8 T cell subsets (central and effector memory) expressed more NE receptors (beta-2 adrenergic receptor) and were significantly more reduced in mRNA (p
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