HTLV-I virological and histopathological analysis in two cases of anti-centromere-antibody-seropositive Sjogrens syndrome
Modern Rheumatology, 05/11/2012
Nakamura H et al. – A high HTLV–I viral load in situ is supposed to promote the production of cytokines, especially TGF–β, resulting in the fibrous change of labial salivary gland (LSG) in anti–centromere–antibody (ACA)–seropositive Sjögren’s syndrome (SS) patients.
One patient was an HTLV–I carrier whereas the other was diagnosed with HTLV–I–associated myelopathy (HAM).
Background data including serum HTLV–I titers, viral loads, and cytokine profiles were recorded.
Azocarmine with aniline blue (Azan)–Mallory staining and immunohistochemistry of the labial salivary glands (LSGs) and a muscle biopsy specimen from the HAM patient were performed.
Serum transforming growth factor beta (TGF–β), tumor necrosis factor alpha (TNF–α), and HTLV–I viral load were high in the HAM–SS patient compared with the HTLV–I carrier.
Fibrous change in LSG was prominent in the HAM–SS patient.
Although TGF–β expression was similar in the two patients, expression of HTLV–I–related proteins including p12, p28, group–specific antigen (GAG), and nuclear factor kappa–B (NF–κB) in the LSG were dominantly detected in the HAM–SS patient.
Frequency of TGF–β staining in HTLV–I–seropositive SS patients without ACA, HTLV–I–seronegative SS patients with ACA, and HTLV–I–seronegative SS patients without ACA was lower than that of the previous two patients.
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