http://www3.interscience.wiley.com/cgi-bin/abstract/86511539/START
Journal of Neuroscience Research
Volume 66, Issue 3, 2001. Pages:
517-524
M. Vergelli 1, B. Mazzanti 1, E.
Traggiai 1, T. Biagioli 1, C. Ballerini 1, A. Parigi 1, A. Konse 2, G.
Pellicanò 2, L. Massacesi 1 *
1Department of Neurology and Psychiatry,
University of Florence, Florence, Italy
2Department of Clinical Physiopathology,
University of Florence, Florence, Italy
Abstract
T cells reactive to self-antigens
are present in the peripheral blood of patients with autoimmune diseases
as well as in healthy subjects.
Although T cell-response to the self-myelin
antigen myelin basic protein (MBP) has been widely investigated in multiple
sclerosis (MS) patients, very little is known about the evolution over
time of this response and its correlation with the disease activity.
In recent years magnetic resonance
imaging (MRI) techniques have provided new tools for following the inflammatory
activity in the central nervous system (CNS) of MS patients.
In the present study the T cell response
to MBP was longitudinally investigated in terms of frequency, epitope specificity,
and cytokine production profile in four patients with relapsing-remitting
MS enrolled in a gadolinium-enhanced MRI serial study.
In spite of different profiles of
inflammatory activity within the CNS, all the patients examined showed
major changes in their reactivity to MBP during the follow-up period in
terms of both frequency and epitope specificity.
Episodic expansions of MBP-specific
T cell populations were observed in each patient, and overall they did
not correlate with disease activity.
In these patients the expansions:
1) occurred in the context of a steady
level of disease activity,
These results suggest that the evolution
over time of the T cell response to a self-antigen such as MBP is more
complex than previously expected.
The short-term repertoire dynamics
of autoreactive T cells in MS underscore the importance of longitudinal
studies for evaluating autoreactivity to myelin antigens and probably to
any self-antigen in other autoimmune diseases.
J. Neurosci. Res. 66:517-524, 2001.
© 2001 Wiley-Liss, Inc.
2) correlated with a burst of CNS
inflammation,
3) followed the appearance of a
new active lesion, and
4) were observed even in the absence
of detectable signs of CNS inflammation during the entire follow-up period.