{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T07:24:10Z","timestamp":1792740250973,"version":"4.5.0"},"reference-count":28,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,5,5]],"date-time":"2004-05-05T00:00:00Z","timestamp":1083715200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2004,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Recent data indicate that molecular mimicry may play a role in the pathogenesis of human\u2010T\u2010lymphotropic virus type\u20101 (HTLV\u20101)\u2010associated myelopathy\/tropical spastic paraparesis (HAM\/TSP), an immune\u2010mediated disease of the central nervous system (CNS). Specifically, HAM\/TSP patients developed antibodies that cross\u2010react with heterogeneous nuclear ribonuclear protein A1 (hnRNP A1), an antigen highly expressed in neurons. Antibodies to HTLV\u20101\u2010tax cross\u2010reacted with hnRNP A1, suggesting molecular mimicry between the two proteins. In support of this hypothesis, HAM\/TSP IgG and antibodies to hnRNP A1 and HTLV\u20101\u2010tax inhibited neuronal firing, suggesting that these antibodies can be pathogenic. We extended these observations by carrying out studies on over 20 different neurons. We also tested IgG isolated from six different HAM\/TSP patients and two HTLV\u20101 seronegative controls and added experiments that control for antibody isotype, antibody target, and neuron viability. In these studies, IgG was infused into the extracellular space during whole\u2010cell current clamp recordings of neurons. Our results confirm that in contrast to normal IgG, IgG from all HAM\/TSP patients completely inhibited neuronal firing. Affinity\u2010purified antibodies specific for hnRNP A1 and a monoclonal antibody to HTLV\u20101\u2010tax (which reacted with hnRNP A1 and whose epitope overlaps the human immunodominant epitope of tax) also inhibited neuronal firing. Monoclonal antibodies to neurofilament did not change neuronal firing. These data indicate that antibodies to neurons can be pathogenic, that biologic activity can be affected by a cross\u2010reactive epitope between HTLV\u20101\u2010tax and hnRNP A1, and that molecular mimicry may play a role in the pathogenesis of HAM\/TSP. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.20137","type":"journal-article","created":{"date-parts":[[2004,5,5]],"date-time":"2004-05-05T22:06:41Z","timestamp":1083794801000},"page":"82-89","source":"Crossref","is-referenced-by-count":29,"title":["Molecular mimicry: Cross\u2010reactive antibodies from patients with immune\u2010mediated neurologic disease inhibit neuronal firing"],"prefix":"10.1002","volume":"77","author":[{"given":"Franck","family":"Kalume","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sang 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