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Thymocyte Fas expression is dysregulated in myasthenia gravis patients with
anti-acetylcholine receptor antibody
N Moulian, J Bidault, F Truffault, AM Yamamoto, P Levasseur and S Berrih-Aknin
CNRS URA 1159 and the Departement de Chirurgie Thoracique, Hopital
Marie-Lannelongue, Le Plessis Robinson, France.
Myasthenia gravis (MG) is a human autoimmune disease mediated by anti-
acetylcholine receptor (AChR) antibodies. The thymus is probably the site
where the autoimmune response is triggered and maintained. Recent reports
have linked various autoimmune disease with defective Fas expression. We
thus analyzed Fas expression in thymocytes and peripheral blood lymphocytes
(PBL) from MG patients. The proportion of a thymocyte subpopulation with
strong Fas expression (Fas(hi)) was markedly enhanced in MG patients with
anti-AChR antibodies (P < .0003, compared with controls). In this group
of patients, the proportion of CD4+ Fas(hi) and CD4+ CD8+ Fas(hi)
thymocytes were significantly increased (P < .002 for both subsets).
Fas(hi) thymocytes were enriched in activated cells and showed intermediate
CD3 expression. They were preferentially Vbeta5.1-expressing cells,
previously shown to be enriched in potentially autoreactive cells. The
proliferative response of thymocytes from MG patients to peptides from the
AChR was abolished after depletion of Fas(hi) cells. Fas(hi) thymocytes
were sensitive to an agonistic anti-Fas antibody. In peripheral blood,
Fas(hi) lymphocytes proportion was not significantly modified in MG
patients whatever their anti-AChR antibody titer, compared with controls.
Altogether, these results indicate that Fas(hi) thymocytes, which
accumulate in MG patients with anti-AChR antibodies, could be involved in
the autoimmune response that targets the AChR.
Volume 89,
Issue 9,
pp. 3287-3295,
05/01/1997
Copyright © 1997 by The American Society of Hematology
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