1997
DOI: 10.1136/ard.56.6.390
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Immunohistochemistry of minor salivary gland biopsy specimens from patients with Sjogren's syndrome with and without hepatitis C virus infection

Abstract: Conclusions-HCV infected patients may develop an autoimmune sialadenitis, similar to that described in primary SS.

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Cited by 45 publications
(15 citation statements)
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“…In our study the evidence of epithelial CD25 expression confirms the previous unusual results of other authors [18,28], but the meaning of this finding remains uncertain, despite its relationship with lymphocyte CD25 and epithelial HLA-DR expression. Also, in our study the correlation between CD25 and HLA-DR expression on lymphocytes and epithelial cells agrees with previous reports showing the coexpression of these activation markers on LSG in SS [18,27]. This could be explained by the fact that IL-2R is necessary for the biologic effects of IL-2 [29], which induces the release of several lymphokines, including g-interferon [30], which in turn promotes HLA-DR synthesis [11,31].…”
Section: Discussionsupporting
confidence: 93%
See 1 more Smart Citation
“…In our study the evidence of epithelial CD25 expression confirms the previous unusual results of other authors [18,28], but the meaning of this finding remains uncertain, despite its relationship with lymphocyte CD25 and epithelial HLA-DR expression. Also, in our study the correlation between CD25 and HLA-DR expression on lymphocytes and epithelial cells agrees with previous reports showing the coexpression of these activation markers on LSG in SS [18,27]. This could be explained by the fact that IL-2R is necessary for the biologic effects of IL-2 [29], which induces the release of several lymphokines, including g-interferon [30], which in turn promotes HLA-DR synthesis [11,31].…”
Section: Discussionsupporting
confidence: 93%
“…Nevertheless it must be emphasised that CD25, as well as HLA-DR, expression on LSG lymphocyte infiltrates is not specific for SS, but it also found in other autoimmune sialoadenitis [18,27], whereas epithelial CD25 expression seems to be specific for SS [18,28]. In our study the evidence of epithelial CD25 expression confirms the previous unusual results of other authors [18,28], but the meaning of this finding remains uncertain, despite its relationship with lymphocyte CD25 and epithelial HLA-DR expression.…”
Section: Discussionmentioning
confidence: 99%
“…The nature of the antigen(s) that drives the expansion and differentiation of effector T cells in pSS remains to be fully characterized, but is represented, at least in part, by autoantigens. Both CD4+ T helper (Th) cells and CD8+ (cytotoxic or killer) T cells have been identified in salivary gland lesions [39]. CD4+ T lymphocytes expressing perforin and with cytotoxic activity are also detected (up to 20% of total T cells) [5].…”
Section: T Cell Mediated Immunopathogenesismentioning
confidence: 99%
“…Sjögren's syndrome was primary since it was not associated with another connective tissue disease (mainly systemic lupus erythematosus, rheumatoid arthritis, scleroderma) as defined by the American College of Rheumatology criteria [7,38,43]. As hepatitis C infection may be associated with pathological changes in minor salivary gland biopsy resembling those observed in SS [12], patients with hepatitis C infection were excluded from the study. Patients with cryoglobulinaemia were also excluded because cryoglobulinaemia may be present in up to 20 % of PSS [37,44] and may contribute to the development of a peripheral neuropathy [21].…”
mentioning
confidence: 99%