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Print version ISSN 0120-4157
On-line version ISSN 2590-7379


DOMINGUEZ, Martha C et al. Autoimmune syndrome in the tropical spastic paraparesis/myelopathy associated with human T-lymphotropic virus infections. Biomédica [online]. 2008, vol.28, n.4, pp.510-522. ISSN 0120-4157.

Introduction. Previous reports have given evidence that in tropical spastic paraparesis (TSP)/ human T-lymphotrophic virus (HTLV-I)-associated myelopathy (HAM), an autoimmune process occurs as part of its pathogenesis. Objective. The roles of autoimmunity and the molecular mimicry was evaluated in TSP/HAM patients. Materials and methods. Plasma samples were characterized from patients in the Pacific coastal region of Colombia. Thirty-seven were identified as TSP/HAM, 10 were diagnosed with adult T-cell leukemia virus, 22 were asymptomatic carriers but seropositive for HTLV-I and 20 were seronegative and served as negative controls. Plasmatic levels of the following were determined:  antinuclear antibody (ANA) levels, anticardiolipine-2 (ACL_2), interferon- (IFN-g) and interleukin-4 (IL-4). Using Western blot, the crossreactivity of the seropositive and seronegative samples was evaluated against proteins extracted from several central nervous system components of non infected Wistar rats. The HTLV-I seropositive plasmas were crossreacted with a monoclonal tax (LT4 anti-taxp40) from spinal cord neurons of non infected Wistar rats. Results. Of the TSP/HAM patients, 70.2% were reactive against ANA and 83.8% against ACL-2, in contrast with those ATL and asymptomatic seropositives subjects that were not reactive (P<0.001). Moreover, 70.3% had detectable levels of IFN and 43.2% had detectable IL-4. LT4 anti-taxp40 and plasma of TSP/HAM exhibited cross reactivity with a MW 33-35 kDa protein from the rat spinal cord nuclei. Conclusion. Support was provided for the existence of an autoimmune syndrome mediated by molecular mimicry; the syndrome was responsible for some of the axonal degeneration observed in TSP/HAM patients.

Keywords : paraparesis, spastic; human T-lymphotropic virus 1; primateT-lymphotropic virus 1; spinal cord; autoantibodies; autoimmunity; molecular mimicry.

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