title: IgG in brain correlates with clinicopathological damage in HTLV-1 associated neurologic disease.
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.
  
  
  CONCLUSIONS
  Patients with HAM/TSP develop antibodies specific for neurons and axons that are preferentially damaged in the CNS.
authors.affiliation: Department of Neurology, University of Tennessee Health Sciences Center, Memphis, TN 38163, USA.
authors.forename: M
authors.initials: M
authors.lastname: Jernigan
authors.forename: Y
authors.initials: Y
authors.lastname: Morcos
authors.forename: S M
authors.initials: SM
authors.lastname: Lee
authors.forename: F C
authors.initials: FC
authors.lastname: Dohan
authors.forename: C
authors.initials: C
authors.lastname: Raine
authors.forename: M C
authors.initials: MC
authors.lastname: Levin
mesh_terms: D000870:Anterior Horn Cells / Q000276:immunology; D000918:Antibody Specificity; D001323:Autoantibodies / Q000032:analysis*; D001324:Autoantigens / Q000276:immunology*; D001369:Axons / Q000276:immunology; D001921:Brain / Q000276:immunology* / Q000473:pathology; D003711:Demyelinating Diseases / Q000209:etiology / Q000276:immunology / Q000473:pathology; D000076245:Heterogeneous Nuclear Ribonucleoprotein A1; D034481:Heterogeneous-Nuclear Ribonucleoprotein Group A-B / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis*; D018716:Molecular Mimicry; D009419:Nerve Tissue Proteins / Q000276:immunology*; D009474:Neurons / Q000276:immunology; D015493:Paraparesis, Tropical Spastic / Q000150:complications / Q000276:immunology* / Q000473:pathology; D013116:Spinal Cord / Q000276:immunology / Q000473:pathology
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D000076245:Heterogeneous Nuclear Ribonucleoprotein A1; D034481:Heterogeneous-Nuclear Ribonucleoprotein Group A-B; D007074:Immunoglobulin G; D009419:Nerve Tissue Proteins; C000619656:hnRNPA1 protein, human