The NK cell as a new player in the pathogenesis of HTLV-I associated neurologic disease.

摘要: 8 Virulence Volume 1 issue Human T-cell lymphotropic virus type I (HTLV-I) is an exogenous human retrovirus that has been demonstrated to be the etiologic agent in adult T cell leukemia and a progressive neurological disease termed HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HAM/TSP caused by preferential damage of thoracic spinal cord characterized clinically muscle weakness, hyperreflexia, spasticity lower extremities, urinary disturbance. It clinical similarities primary form multiple sclerosis. Although development not completely understood, virus-host immunological interactions have suggested play role pathogenesis this disorder. A number functions shown elevated patients with HAM/TSP, including high frequencies circulating HTLV-I-specific CD8+ cytotoxic lymphocytes (CTL), antibody titers against HTLV-I antigens both peripheral blood cerebrospinal fluid, increased expression cytokine chemokines. The hallmark infected individuals capacity PBMC spontaneously proliferate vitro, i.e., extraordinarily uptake 3H-thymidine (typically greater than 100,000 cpm after 4 days culture) absence or stimulants. Moreover, magnitude spontaneous lymphoproliferation more pronounced asymptomatic carriers used as evaluation treatment for Since proviral load typically higher nK new player HtLV-i associated neurologic