In the labial salivary glands (LSGs) of 16 primary and 18 secondary Sjögren's syndrome (SS) patients, infiltrating lymphocytes were histologically and immunohistochemically examined; also, the serum levels of rheumatoid factor, antinuclear antibodies, anti-DNA antibodies, anti-SS-A and anti-SS-B antibodies, and immunoglobulins (including IgG, IgM and IgA) were all assayed. An immunohistochemical analysis of the lymphocyte subsets in LSGs revealed that severe lymphocytic infiltration was frequently accompanied by marked B cell accumulation both in primary and secondary SS patients. Furthermore, local B cell accumulation was also closely associated with elevated levels of anti-SS-A and anti-SS-B antibodies and IgG, and this association was statistically significant in the group with primary SS but not in the group with secondary SS. Thus, local lymphocytic infiltration, especially B cell accumulation, in the salivary glands is suggested to be involved in serological abnormalities in primary SS, while complicated autoimmune diseases other than SS may also be involved in serological abnormalities in secondary SS.

Objective. To clarify the involvement of human T lymphotropic virus type I (HTLV-I) in the pathogenesis of Sjogren's syndrome (SS). Methods. In HTLV-I-seropositive patients with SS, HTLV-I proviral DNA in the labial salivary glands (SG) was detected by polymerase chain reaction (PCR) amplification of the extracted cellular DNA, and the localization in the SG was examined by in situ PCR hybridization. Results. The cellular DNA extracted from the SG contained full HTLV-I proviral DNA, which was present in the nucleus of the infiltrating T cells, but not in either the SG epithelial cells or the acidar cells. Furthermore, the viral loads in the SG were-8 times to 9 X lo3 times higher than those in the peripheral blood mononuclear cells. Conclusion. Accumulation of HTLV-I-infected T cells in the SG suggests that HTLV-I likely causes the self-reactive T cells to proliferate, which, as a result, induces SS. Human T lymphotropic virus type I (HTLV-I) was originally identified as a causative agent of adult T