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Neurology 2003;60:1320-1327
© 2003 American Academy of Neurology

IgG in brain correlates with clinicopathological damage in HTLV-1 associated neurologic disease

M. Jernigan, BA, Y. Morcos, PhD, S.M. Lee, PhD, F.C. Dohan, Jr., MD, C. Raine, PhD and M.C. Levin, MD

From the Department of Neurology (M. Jernigan, and Drs. Morcos, Lee, and Levin), Neuroscience Center (Drs. Morcos, Lee, and Levin), and Department of Pathology (Dr. Dohan), University of Tennessee Health Sciences Center, Memphis; Research Service (Drs. Lee and Levin), Veterans Affairs Medical Center (VAMC), Memphis, TN; and Department of Neuropathology (Dr. Raine), Albert Einstein College of Medicine, Bronx, NY.

Address correspondence and reprint requests to Dr. Michael C. Levin, Associate Professor, Department of Neurology, University of Tennessee Health Sciences Center, Link Building, Room 415, 855 Monroe Avenue, Memphis, TN 38163; e-mail: mlevin{at}utmem.edu

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.




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