The immunopathogenesis of the HTLV-I associated myelopathy (HAM) may be studied by the CSF evaluation. The mechanism of this myelopathy remains unknown. The disturbs of the cellular and humoral immune response observed in HAM patients suggest that the immunological derangement may contribute to the disease mechanisms. For hypothesis, the migration of infected lymphocytes through the blood-brain barrier could have a main role at the pathogenesis of HAM. An increase of the production of cytokines as tumor necrosis factor alpha (TNF alpha) contributes to the migration of lymphocytes through the expression of the intercellular adhesion molecule on the surface of the endothelial cells. On the other side, new knowledges suggest that the imbalance between the production of TNF alpha and its soluble receptor (sTNF-R) could result in the lesive effects of this cytokine in the central nervous system.
HTLV-I retrovirus; cerebrospinal fluid; central nervous system; myelopathy; cytokines; sTNF-R