Abstract HTLV-I has been identified as a causative agent which initiates and/or perpetuates the process of Sjogren's syndrome (SS) and rheumatoid arthritis (RA). A high seroprevalence of HTLV-I infection has been determined in both SS and RA patients in the HTLV-I-endemic area of Nagasaki, Japan. HTLV-I proviral DNA and HTLV-I Tax/Rex mRNA are expressed in the salivary glands or synovial cells of HTLV-I-seropositive SS or RA patients, indicating that HTLV-I is present in the affected organs and modulates the process of the disease. Cellular functions are modulated by HTLV-I infection, showing that cell proliferation and cytokine production are upregulated in HTLV-I-infected cells, and this is in part mediated by the HTLV-I Tax-induced NF-3B activation of host cells. Furthermore, Tax-mediated NF-3B activation involves resistance toward apoptotic stimuli in HTLV-I infected cells. These modulatory effects of HTLV-I Tax are believed to be important in promoting autoimmune disorders such as SS and RA in HTLV-I-seropositive subjects.
