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Abstract
Objective: To test the authors’ hypothesis that antibody deposition in autopsy specimens from patients with human T-lymphotropic virus type 1–associated myelopathy/tropical spastic paraparesis (HAM/TSP) would correlate with CNS damage.
Methods: Endogenous immunoglobulin G (IgG) was detected using antihuman IgG in autopsy tissues from HAM/TSP and control patients. IgG was isolated from the CSF, CNS, and sera of patients with HAM/TSP and tested for reactivity to heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1), an autoantigen recently associated with molecular mimicry in HAM/TSP.
Results: In situ IgG localized to elements of the corticospinal system including neurons of the frontal cortex and precentral gyrus, as well as throughout axons in subcortical white matter, periventricular white matter, posterior limb of the internal capsule, midbrain, pons, and medulla. Similarly, there was IgG deposition within the posterior-column/medial lemniscal sensory system, including the arcuate fibers of the cranial-cervical junction, the nucleus cuneatus, and throughout the course of the medial lemniscus in the medulla, pons, and midbrain. IgG from brain, CSF, and serum of the patients with HAM/TSP showed immunoreactivity with hnRNP A1.
Conclusion: Patients with HAM/TSP develop antibodies specific for neurons and axons that are preferentially damaged in the CNS.
- Received October 9, 2002.
- Accepted January 18, 2003.
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