Extended report
Glandular and extraglandular expression of costimulatory
molecules in patients with Sjögren's syndrome
R Matsumuraa, K Umemiyaa, T Gotoa, T Nakazawaa, M Kagamia, H Tomiokaa, E Tanabeb, T Sugiyamac, M Sueishic
a Department of
Internal Medicine, Toho University School of Medicine, Sakura Hospital,
Japan, b Department of Dermatology, Toho University
School of Medicine, c Department
of Internal Medicine, National Shimoshizu Hospital, Japan
Correspondence to: Dr R Matsumura, Department of Internal Medicine, Toho University School of Medicine, Sakura Hospital, 5641 Shimoshizu, Sakura City, Chiba 285-8741, Japan ryu-ma{at}ka2.so-net.ne.jp
Accepted for publication 20 October
2000
OBJECTIVES
To
investigate the expression and regulation of CD80, CD86, and CD28
costimulatory molecules in sialoadenitis and interstitial nephritis in
patients with Sjögren's syndrome (SS).
METHODSExpression of
CD80, CD86, and CD28 molecules was studied by immunohistochemical
staining of lip biopsy specimens obtained from patients who had
sialoadenitis associated with SS, and renal biopsy specimens obtained
from patients who had interstitial nephritis associated with SS. To
elucidate the mechanism of de novo expression of CD80 and CD86
antigens, their induction by cytokines in human salivary duct cell line
(HSG) and renal cortical epithelial cells (HRCE) by cell enzyme linked
immunosorbent assay (ELISA) was quantitatively investigated.
RESULTSIn patients
with severe sialoadenitis, CD80 and CD86 were strongly expressed on
ductal epithelial cells. In contrast, these antigens were not found in
the minor salivary glands of normal subjects or of patients with mild
sialoadenitis. Some infiltrating cells expressed CD28. In patients who
had interstitial nephritis associated with SS, some tubular epithelial
cells expressed CD86 but not the CD80 antigen. Unstimulated HSG cells
did not express CD80 or CD86. Interferon 
(IFN) consistently up
regulated levels of CD80 and CD86. In contrast, tumour necrosis factor
(TNF), interleukin 1
(IL1), IL2, and IL4 had no effect on
either CD80 or CD86 levels. Unstimulated HRCE did not express CD80 or
CD86. IFN consistently up regulated CD86 expression. No CD80
expression was found on tubular cells. TNF, IL1, IL2, and IL4 had
no discernible effects.
CONCLUSIONSSalivary
ductal cells in patients with SS can express CD80 and CD86
costimulatory molecules in response to IFN. Tubular epithelial cells
in patients who have interstitial nephritis associated with SS express
only CD86 molecules. In patients with SS, salivary ductal cells and
tubular epithelial cells may activate infiltrating CD28 positive T
lymphocytes by presenting antigens to T cells, potentially leading to
tissue destruction.
© 2001 by Annals of the Rheumatic Diseases
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