J. Coll et al., IMMUNOHISTOCHEMISTRY OF MINOR SALIVARY-GLAND BIOPSY SPECIMENS FROM PATIENTS WITH SJOGRENS-SYNDROME WITH AND WITHOUT HEPATITIS-C VIRUS-INFECTION, Annals of the Rheumatic Diseases, 56(6), 1997, pp. 390-392
Objectives-To characterise phenotypically the minor salivary glands of
patients with clinical and histological features of Sjogren's syndrom
e (SS) infected with hepatitis C virus (HCV). Patients and Methods-75
consecutive patients with SS (31 primary SS, 44 secondary SS) diagnose
d by preliminary classification criteria. The of anti-HCV antibodies w
as detected by commercial third generation ELISA and by a second gener
ation immunoblot assay. Presence of HCV genome in serum was determined
by polymerase chain reaction analysis. Expression of CD3, CD4, CD8, C
D20, HLA-DR, and CD25 molecules in lymphocytic and epithelial cells on
minor salivary glands was detected by immunohistochemical assays. Exp
ression of interferon gamma and interleukin 4 cytokines was determined
by in situ hybridisation. Results-Six of 31 primary SS (19%) and one
of 44 secondary SS (2%) serum samples were positive for anti-HCV by EL
ISA. Three samples were positive, three indeterminate, and one sample
corresponding to a secondary SS patient was negative by immunoblot. Th
e three immunoblot positive serum samples were also HCV-RNA positive b
y PCR assay. The study of lymphocytic cells in the diffuse infiltrate
of minor salivary glands showed a predominance of the CD3 lymphocytic
population. A predominance of CD4 over CD8 T cells (ratio 2:1) was obs
erved in HCV and non- HCV infected patients. The analysis of the lymph
ocytic focus showed that the HCV infected patients had a predominance
of CD20 positive cells. Activation molecules ( CD-25 and HLA-DR) were
expressed in HCV and non-HCV infected patients in lymphocytic and epit
helial cells, however epithelial cell expression of CD25 was low in HC
V infected patients. As expected, a pronounced Th1 response was observ
ed in the lymphocytic foci of HCV patients. Conclusions-HCV infected p
atients may develop an autoimmune sialadenitis, similar to that descri
bed in primary SS.