{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T21:41:42Z","timestamp":1789940502590,"version":"4.0.1"},"reference-count":43,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T00:00:00Z","timestamp":1097193600000},"content-version":"vor","delay-in-days":2291,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[1998,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Molecular mimicry is implicated in the pathogenesis of autoimmune diseases such as diabetes mellitus, rheumatoid arthritis, and multiple sclerosis (MS). Cellular and antibody\u2010mediated immune responses to shared viral\u2010host antigens have been associated with the development of disease in these patients. Patients infected with human T\u2010lymphotropic virus type I (HTLV\u2010I) develop HTLV\u2010I\u2010associated myelopathy\/tropical spastic paraparesis (HAM\/TSP), an immunemediated disorder of the central nervous system (CNS) that resembles some forms of MS. Damage to neuronal processes in the CNS of HAM\/TSP patients is associated with an activated cellular and antibody\u2010mediated immune response. In this study, IgG isolated from HAM\/TSP patients was immunoreactive with uninfected neurons and this reactivity was HTLV\u2010I specific. HAM\/TSP IgG stained uninfected neurons in human CNS and cell lines but not nonneuronal cells. Neuronal western blots showed IgG reactivity with a single 33\u2010kd band in all HAM\/TSP patients tested. By contrast, no neuron\u2010specific IgG reactivity could be demonstrated from HTLV\u2010I seronegative controls and, more important, from HTLV\u2010I seropositive, neurologically asymptomatic individuals. Both immunocytochemical staining and western blot reactivity were abolished by preincubating HAM\/TSP IgG with HTLV\u2010I protein lysate but not by control proteins. Staining of CNS tissue by a monoclonal antibody to HTLV\u2010I tax (an immunodominant HTLV\u2010I antigen) mimicked HAM\/TSP IgG immunoreactivity. There was no staining by control antibodies. Absorption of HAM\/TSP IgG with recombinant HTLV\u2010I tax protein or preincubation of CNS tissue with the monoclonal antibody to HTLV\u2010I tax abrogated the immunocytochemical and western blot reactivity of HAM\/TSP IgG. Furthermore, in situ human IgG localized to neurons in HAM\/TSP brain but not in normal brain. These data indicate that HAM\/TSP patients develop an antibody response that targets uninfected neurons, yet reactivity is blocked by HTLV\u2010I, suggesting viral\u2010specific autoimmune reactivity to the CNS, the damaged target organ in HAM\/TSP.<\/jats:p>","DOI":"10.1002\/ana.410440115","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T15:17:07Z","timestamp":1104592627000},"page":"87-98","source":"Crossref","is-referenced-by-count":47,"title":["Neuronal molecular mimicry in immune\u2010mediated neurologic disease"],"prefix":"10.1002","volume":"44","author":[{"given":"Michael 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