Extended reports
A comparative phenotypical analysis of rheumatoid nodules and
rheumatoid synovium with special reference to adhesion molecules and
activation markers
a Departments
of Rheumatology, b and Pathology, c University Hospital Ghent, Belgium
Correspondence to: Dr F De Keyser, Department of Rheumatology 0K12IB, University Hospital Ghent, De Pintelaan 185, 9000 Ghent, Belgium.
Accepted for publication 11 June 1998
OBJECTIVES
(1)To
analyse the in situ expression of adhesion molecules in rheumatoid
nodules. (2) To compare the endothelial expression of adhesion
molecules in synovial tissue and subcutaneous nodules obtained from the
same patients. (3) To compare the expression of adhesion molecules and
activation markers on T cell lines from nodules and synovium.
METHODS(1)
Immunohistochemical analysis by APAAP technique of E selectin, CD44,
ICAM-1, PECAM-1, and VCAM-1 was performed on 10 rheumatoid nodules from
seven patients with rheumatoid arthritis (RA); nodules and synovium
were simultaneously analysed from three patients. (2) T cell lines were
generated from RA nodules (n=7) and synovium (n=7) by interleukin 2 expansion, and subsequently characterised by flow cytometry for surface
expression of 
E
7, 47, CD44, L selectin, LFA-1a, PECAM-1,
and CD30.
RESULTS(1) In
rheumatoid nodules, the palisading layer strongly stains for ICAM-1 and
PECAM-1, but less pronounced for CD44. VCAM-1 staining was usually
negative. ICAM-1 is upregulated in the vessels surrounding the central
zone of fibrinoid necrosis. The immunohistological picture in different
nodules derived from the same patient was similar. (2) The endothelial
expression of adhesion molecules is comparable in RA nodules and
synovium on an individual level, except for E selectin, which is
overexpressed in nodule endothelium. (3) T cell lines from nodules and
synovium display similar adhesion molecule profiles. However, the
expression of CD30, a T cell activation marker linked with Th2 subsets,
is higher in nodules compared with synovium.
CONCLUSIONThese data
support a recirculation hypothesis of T cells between articular and
extra-articular manifestations in RA, although the activation state of
the T cells in each of these localisations may differ.
© 1998 by Annals of the Rheumatic Diseases
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