[Immunological analysis of HTLV-I env-pX transgenic rat with various collagen vascular diseases].

Human T lymphocyte virus type-I (HTLV-I) is an etiologic agent of not only adult T cell leukemia but also HTLV-I associated myelopathy/tropical spastic paraparesis, HTLV-I associated arthropathy and other immunological disorders, such as Sjögren syndrome, dermatitis, polymyositis, and uveitis. We recently reported that a wide spectrum of collagen vascular diseases, including inflammatory arthropathy resembling rheumatoid arthritis, myocarditis, dermatitis, necrotizing arteritis, myositis and sialoadenitis similar to Sjögren's syndrome, developed in the transgenic rat carrying HTLV-I env-pX region under the control of its own long terminal repeat (env-pX rat). To investigate the pathogenetic role of these diseases, cell surface molecules and functions of lymphocytes from env-pX rats were examined in this study. In env-pX rats with diseases, not only infiltrating lymphocytes in the inflammatory sites but also peripheral lymphocytes expressed a large number of co-stimulating molecules such as CD80/86 and ICAM-1, compared with those of normal rats or rats with adjuvant-induced arthritis or myosin-induced myocarditis. Moreover, the expression of CD80/86 and ICAM-1 was already up-regulated on the surface of peripheral lymphocytes in env-pX rat before developing any diseases. Lymphocytes, taken from env-pX rats immunized with myosin in vivo, showed significantly higher cellular response against myosin in vitro than those of normal rats. Lymphocytes from env-pX rats also showed the hyper-reactivity to the stimulation by super-antigens, but no significant difference of the usage of T cell receptor V beta was found compared with those of normal rats. These results suggest that the env-pX transgene may induce the high expression of CD80/86 and ICAM-1 on the lymphocytes and the resulting hyper-immune responsiveness in env-pX rats.