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The Journal of Immunology, 2001, 166: 232-240.
Copyright © 2001 by The American Association of Immunologists

IFN-{gamma} Production by Th1 Cells Generated from Naive CD4+ T Cells Exposed to Norepinephrine1

Michelle A. Swanson*, William T. Lee{ddagger} and Virginia M. Sanders2,*,{dagger}

Departments of * Microbiology and Immunology, and {dagger} Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL 60153; and {ddagger} Department of Immunology, Wadsworth Institute, Albany, NY 12208

During activation in vivo, naive CD4+ T cells are exposed to various endogenous ligands, such as cytokines and the neurotransmitter norepinephrine (NE). To determine whether NE affects naive T cell differentiation, we used naive CD4+ T cells sort-purified from either BALB/c or DO11.10 TCR-transgenic mouse spleens and activated these cells with either anti-CD3/anti-CD28 mAbs or APC and OVA323–329 peptide, respectively, under Th1-promoting conditions. RT-PCR and functional assays using selective adrenergic receptor (AR) subtype antagonists showed that naive CD4+ T cells expressed only the {beta}2AR subtype to bind NE and that stimulation of this receptor generated Th1 cells that produced 2- to 4-fold more IFN-{gamma}. This increase was due to more IFN-{gamma} produced per cell upon restimulation instead of more IFN-{gamma}-secreting cells, as determined by IFN-{gamma}-specific immunofluorescence and enzyme-linked immunospot. In contrast, Th1 cell differentiation was unaffected when naive T cells were exposed to NE and activated either in the presence of a neutralizing anti-IL-12 mAb or by APC from IL-12-deficient mice. Moreover, the addition of IL-12 to the IL-12-deficient APC cultures restored the ability of NE to increase Th1 differentiation. Taken together, these results indicate that a possible link may exist between the signaling pathways used by NE and IL-12 to increase naive CD4+ T cell differentiation to a Th1 cell.




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