From: Kofi on
To say the least, I've been thinking the same thing for two or three
years now. Those with locally damaged sympathetic nerves, though, will
have to regenerate those nerves as part of any "cure" for this class of
autoimmunity.

Brain Behav Immun. 2010 Feb;24(2):186-92. Epub 2009 Jul 16.

The B cell, arthritis, and the sympathetic nervous system.
Pongratz G, Straub RH.
Laboratory of Experimental Rheumatology and Neuroendocrino-Immunology,
Department of Internal Medicine I, University Hospital Regensburg, 93042
Regensburg, Germany.

The pathogenesis of rheumatoid arthritis (RA) is still an unresolved
puzzle. Many factors and inflammatory cells play together to initiate a
chronic inflammatory process that, if untreated, leads to complete
destruction of involved joints. Recent success in treating severe forms
of RA with B cell-depleting or -modifying agents revived the concept
that the B cell might play a pivotal role in the pathogenesis of some
forms of arthritis. However, the rather unspecific treatment approach
affecting all B cells, no matter if autoreactive or not, leads to
potential harmful side-effects, e.g., severe infections. Therefore,
finding regulatory systems that more specifically modulate B cell
function is important to improve current treatment options. One such
regulatory system is the sympathetic nervous system (SNS), which is
known to modulate B cell function, but also profoundly influences
arthritis development and severity. This review develops the hypothesis
that the SNS via modulating B cell function influences arthritis
development and progression. For this purpose data is presented that
shows (1) how the SNS influences B cell function, (2) how the SNS
influences arthritis development and severity, and (3) how B cells are
involved in the disease process with an emphasis on possible contact
points for SNS neuromodulation. Copyright 2009 Elsevier Inc. All rights
reserved.

Publication Types:
* Review

PMID: 19616611