{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T13:46:54Z","timestamp":1773409614978,"version":"3.50.1"},"reference-count":35,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T00:00:00Z","timestamp":1104537600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,1,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Multiple sclerosis (MS) is an autoimmune CNS demyelinating disease in which infection may be an important initiating factor. Pathogen-induced cross-activation of autoimmune T cells may occur by molecular mimicry. Infection with wild-type Theiler\u2019s murine encephalomyelitis virus induces a late-onset, progressive T cell-mediated demyelinating disease, similar to MS. To determine the potential of virus-induced autoimmunity by molecular mimicry, a nonpathogenic neurotropic Theiler\u2019s murine encephalomyelitis virus variant was engineered to encode a mimic peptide from protease IV of Haemophilus influenzae (HI), sharing 6 of 13 aa with the dominant encephalitogenic proteolipid protein (PLP) epitope PLP139\u2013151. Infection of SJL mice with the HI mimic-expressing virus induced a rapid-onset, nonprogressive paralytic disease characterized by potent activation of self-reactive PLP139\u2013151-specific CD4+ Th1 responses. In contrast, mice immunized with the HI mimic-peptide in CFA did not develop disease, associated with the failure to induce activation of PLP139\u2013151-specific CD4+ Th1 cells. However, preinfection with the mimic-expressing virus before mimic-peptide immunization led to severe disease. Therefore, infection with a mimic-expressing virus directly initiates organ-specific T cell-mediated autoimmunity, suggesting that pathogen-delivered innate immune signals may play a crucial role in triggering differentiation of pathogenic self-reactive responses. These results have important implications for explaining the pathogenesis of MS and other autoimmune diseases.<\/jats:p>","DOI":"10.4049\/jimmunol.174.2.907","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T01:32:54Z","timestamp":1398043974000},"page":"907-917","source":"Crossref","is-referenced-by-count":37,"title":["Viral Delivery of an Epitope from <i>Haemophilus influenzae<\/i> Induces Central Nervous System Autoimmune Disease by Molecular Mimicry"],"prefix":"10.1093","volume":"174","author":[{"given":"J Ludovic","family":"Croxford","sequence":"first","affiliation":[{"name":"Department of Microbiology-Immunology, and Interdepartmental Immunobiology Center, Northwestern University Medical School , Chicago, IL 60611"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Holly A","family":"Anger","sequence":"additional","affiliation":[{"name":"Department of Microbiology-Immunology, and Interdepartmental Immunobiology Center, Northwestern University Medical School , Chicago, IL 60611"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephen D","family":"Miller","sequence":"additional","affiliation":[{"name":"Department of Microbiology-Immunology, and Interdepartmental Immunobiology Center, Northwestern University Medical School , Chicago, IL 60611"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2005,1,15]]},"reference":[{"key":"2025032706130255900_R1","first-page":"382","volume-title":"Clin. 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