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Immunohistochemistry of minor salivary gland biopsy specimens from patients with Sjögren’s syndrome with and without hepatitis C virus infection

Abstract

OBJECTIVES To characterise phenotypically the minor salivary glands of patients with clinical and histological features of Sjögren’s syndrome (SS) infected with hepatitis C virus (HCV).

PATIENTS AND METHODS 75 consecutive patients with SS (31 primary SS, 44 secondary SS) diagnosed by preliminary European classification criteria. The presence of anti-HCV antibodies was detected by commercial third generation ELISA and by a second generation immunoblot assay. Presence of HCV genome in serum was determined by polymerase chain reaction analysis. Expression of CD3, CD4, CD8, CD20, HLA-DR, and CD25 molecules in lymphocytic and epithelial cells on minor salivary glands was detected by immunohistochemical assays. Expression of interferon γ 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 ELISA. Three samples were positive, three indeterminate, and one sample corresponding to a secondary SS patient was negative by immunoblot. The three immunoblot positive serum samples were also HCV-RNA positive by 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 observed in HCV and non- HCV infected patients. The analysis of the lymphocytic 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 epithelial cells, however epithelial cell expression of CD25 was low in HCV infected patients. As expected, a pronounced Th1 response was observed in the lymphocytic foci of HCV patients.

CONCLUSIONS HCV infected patients may develop an autoimmune sialadenitis, similar to that described in primary SS.

  • hepatitis C virus
  • immunohistochemistry
  • Sjögren’s syndrome

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