gentle) exertion/activity of going from home to a hospital appointment was
found to increase TGF-beta (mentioned below) in CFS patients. Ref: White
PD, Nye KE, Pinching AJ, Yap TM, Power N, Vleck V, 10. et al. Immunological
changes after both exercise and activity in chronic fatigue syndrome: a
pilot study. J Chronic Fatigue Syndrome 2004; 12: 51-66. Tom]
http://www.medicalnewstoday.com/articles/172598.php
Link Discovered Between The Nervous And Immune Systems - Might Lead To New
Treatments For Autoimmune Disorders
Main Category: Immune System / Vaccines
Article Date: 01 Dec 2009 - 13:00 PST
If you ever thought the stress of seeing your extended family over the
holidays was slowly killing you - bad news: a new research report in the
December 2009 print issue of the Journal of Leukocyte Biology shows that you
might be right. Here's the good news: results from the same study might lead
to entirely new treatments that help keep autoimmune diseases like lupus,
arthritis, and eczema under control. That's because researchers from the
University of Connecticut Health Center have found that the same part of our
nervous system that is responsible for the fight-or-flight response (called
the sympathetic nervous system) also controls regulatory T cells, which are
used by the body to end an immune response once a foreign invader has been
removed or destroyed.
"We show for the first time that the nervous system controls the central
immune police cells, called regulatory T cells," said Robert E. Cone, Ph.D.,
a senior researcher in whose laboratory the work was done at the University
of Connecticut Health Center. "This further shows that it is imperative to
concentrate on the neuro-immune interactions and to understand how these two
different systems, the immune and nervous systems, interact."
To make this discovery, Cone, Sourojit Bhowmick and colleagues injected some
mice with a drug called 6-hyroxydopamine (6-OHDA) that selectively removes
sympathetic nerves located in different organs, or a saline solution. Mice
injected with 6-OHDA, which effectively severed the link between the nervous
system and the immune system had twice as many regulatory T cells as the
control group in their spleens and lymph nodes. Further analysis showed that
the increase in regulatory T cells resulted from an increase in a protein
called "TGF-beta," which directs the development and survival of regulatory
T cells. With this information in hand, Cone and colleagues then sought to
see if 6-OHDA would prevent autoimmune disorders from developing. To do
this, they injected 6-OHDA or a saline solution into mice before subjecting
them and a control group to conditions known to cause an autoimmune disease
similar to multiple sclerosis in humans. Unlike the control group, the mice
treated with 6-OHDA did not develop the autoimmune disease, showing that not
only can the sympathetic nervous system negatively affect the immune system,
but it also shows how it might be possible to prevent or stop autoimmune
disorders.
"Ever since Hans Seyle's groundbreaking work on stress, scientists have been
trying to understand why stressful situations often exacerbate autoimmune
diseases and cause re-emergence of latent infections," said John Wherry,
Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "In true fight or
flight situations, stress can be a lifesaver, but understanding how the
neurological response to the stress of everyday events such as seeing your
family around the holidays impacts immune responses should provide
opportunities for new therapies."
Details: Sourojit Bhowmick, Anurag Singh, Richard A. Flavell, Robert B.
Clark, James O'Rourke, and Robert E. Cone. The sympathetic nervous system
modulates CD4+FoxP3+ regulatory T cells via a TGF-beta-dependent mechanism.
J Leukoc Biol 2009 86: 1275. doi: 10.1189/jlb.0209107 ;
http://www.jleukbio.org/cgi/content/abstract/86/6/1275
Source:
Cody Mooneyhan
Federation of American Societies for Experimental Biology
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