Immunopathogenesis of HTLV-I-associated myelopathy/tropical spastic paraparesis.

摘要: The main pathological feature of human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is chronic inflammation the spinal cord characterized by perivascular cuffing mononuclear cells accompanied parenchymal lymphocytic infiltration. Although exact mechanism pathogenesis HAM/TSP still obscure, immunological abnormalities arising from a high HTLV-I proviral load in peripheral blood lymphocytes (PBL) play an important role process lesions patients. relationship between HLA haplotype and risk occurrence will be elucidated results studies allele typing. In addition, recent data indicate that its expression are localized infiltrated within patients rather than resident central nervous system (CNS) cells. bystander damage surrounding CNS tissues, which CD8+ HTLV-I-specific cytotoxic T lymphocyte (CTL) attack HTLV-I-infected lymphocytes, might involved events cords HAM/ TSP as one actual pathogenetic mechanisms, heightened transmigrating activity CD4+ to tissues may have key development HAM/TSP. Therefore, although underlying PBL unknown, we must consider therapeutic approaches eliminate lymphocytes.