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Excerpt
We have described the clinical characteristics and immunopathologic features in HTLV-I-infected patients presenting with chronic inflammatory arthropathy and immune dysregulation. These findings allowed us to investigate that HTLV-I may potentially induce complex disease spectra which manifest as primary autoimmune disorders. Further investigations from our laboratory revealed that the HTLV-I tax gene, known as a transregulatory gene, contributes not only to the induction of synovial cell hyperplasia, but also to the immune response, both in vivo and in vitro. The results based on these studies strongly suggest that HTLV-I is the etiologic agent in HTLV-I-associated autoimmune disorders. In this conference, we describe the results of current studies from our laboratory as well as from others, suggesting that HTLV-I plays a critical role as a causative agent of destructive arthropathy and other immune dysfunctions, such as Sjögren's syndrome (SS) and polymyositis based on molecular genetics analysis.
