The vagus nerve modulates CD4+ T cell activity |
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| Authors: | Khalil Karimi John Bienenstock Lu Wang Paul Forsythe |
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| Affiliation: | 1. Department of Pathology and Human Anatomy, Loma Linda University, School of Medicine, Loma Linda, CA, 92350, USA;2. College of Arts and Sciences, Kent State University and the Kent Summa Initiative for Clinical and Translational Research, Summa Health System, Akron, OH 44304, USA;1. Department of Dermatology, University of California, Irvine, CA 92697, USA;2. Department of Molecular Pharmacology, Kitasato University School of Pharmacy, Tokyo 108-8641, Japan;3. Institute of Pathology, University Medical Center, Johannes Gutenberg-University, Mainz D-55101, Germany;4. Institute for Anatomy and Cell Biology, Justus-Liebig-University, Giessen D-35385, Germany;1. Division of Trauma, Surgical Critical Care, and Burns, Department of Surgery, University of California San Diego Health Sciences, San Diego, CA, United States;2. Universidade de Brasilia, DF, Brazil |
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| Abstract: | The vagus nerve has a counter-inflammatory role in a number of model systems. While the majority of these anti-inflammatory effects have been ascribed to the activation of nicotinic receptors on macrophages, little is known about the role of the vagus in modulating the activity of other cells involved in inflammatory responses. Here, we demonstrate that following subdiaphragmatic vagotomy of mice CD4+ T cells from the spleen proliferated at a higher rate and produced more pro-inflammatory cytokines, including TNF and IFN-γ, upon in vitro stimulation. Cell responses were restored to control levels following the administration of nicotine and the treatment of non-vagotomized animals with a nicotinic receptor antagonist could mimic the effect of vagotomy. Our results suggest that vagal input constitutively down-regulates T cell function through action at nicotinic receptors and the role of the vagus in regulating immune responses is more extensive than previously demonstrated. |
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