Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.0209107 on September 9, 2009

Published online before print September 9, 2009
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Buy
Right arrow All Versions of this Article:
jlb.0209107v1
86/6/1275    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Google Scholar
Right arrow Articles by Bhowmick, S.
Right arrow Articles by Cone, R. E.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bhowmick, S.
Right arrow Articles by Cone, R. E.
Related Collections
Right arrowRelated Article
(Journal of Leukocyte Biology. 2009;86:1275-1283.)
© 2009 Society for Leukocyte Biology

The sympathetic nervous system modulates CD4+FoxP3+ regulatory T cells via a TGF-β-dependent mechanism

Sourojit Bhowmick*, Anurag Singh*, Richard A. Flavell{dagger}, Robert B. Clark*, James O'Rourke* and Robert E. Cone*,1

* Department of Immunology, University of Connecticut Health Center, Farmington, Connecticut, USA; and
{dagger} Department of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut, USA

1. Correspondence: Department of Immunology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT 06030, USA. E-mail: cone{at}uchc.edu

ABSTRACT

CD4+FoxP3+ Tregs are essential mediators of the peripheral immune response to self-antigens. Accordingly, the homeostatic regulation of Treg activity and number would impact on the immune response to both self- and non-self antigens. Because the sympathetic nervous system (SNS) interacts chemically and physically with the central and peripheral immune system and exerts a direct influence on antigen-presenting cells and effector lymphocytes, we have investigated the effect of chemical ablation of the SNS on the number and function of peripheral Treg. Removal of murine peripheral sympathetic innervation by 6-hydroxydopamine induced an increase in splenic and lymph node CD4+FoxP3+ Tregs by a TGF-β-dependent mechanism. Further, this increase in Tregs coincides with an inhibition of the induction of experimental autoimmune encephalomyelitis. Our results demonstrate that the SNS is an important contributor to the maintenance of peripheral Treg and TGF-β acts as a bridge between the immune system and the nervous system. Neurological events mediated by the SNS, such as a stress response, may affect the number of T cells that regulate an immune response. Additionally, targeting Tregs via the SNS may be a novel approach to the prevention or treatment of autoimmune diseases.

Key Words: EAE • neuroimmunology • sympathectomy


Related Article

Editorial: Regulation of the regulator: sympathetic nervous system control of regulatory T cells
Kristie M. Grebe
J. Leukoc. Biol. 2009 86: 1269-1270. [Full Text] [PDF]



This article has been cited by other articles:


Home page
J. Leukoc. Biol.Home page
K. M. Grebe
Editorial: Regulation of the regulator: sympathetic nervous system control of regulatory T cells
J. Leukoc. Biol., December 1, 2009; 86(6): 1269 - 1270.
[Full Text] [PDF]