{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,4]],"date-time":"2026-07-04T03:19:02Z","timestamp":1783135142422,"version":"3.54.6"},"reference-count":93,"publisher":"MDPI AG","issue":"1","license":[{"start":{"date-parts":[[2015,12,24]],"date-time":"2015-12-24T00:00:00Z","timestamp":1450915200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Viruses"],"abstract":"<jats:p>Human T-lymphotropic virus type-1 (HTLV-1) infection is associated with adult T-cell leukemia\/lymphoma (ATL). Tropical spastic paraparesis\/HTLV-1-associated myelopathy (PET\/HAM) is involved in the development of autoimmune diseases including Rheumatoid Arthritis (RA), Systemic Lupus Erythematosus (SLE), and Sj\u00f6gren\u2019s Syndrome (SS). The development of HTLV-1-driven autoimmunity is hypothesized to rely on molecular mimicry, because virus-like particles can trigger an inflammatory response. However, HTLV-1 modifies the behavior of CD4+ T cells on infection and alters their cytokine production. A previous study showed that in patients infected with HTLV-1, the activity of regulatory CD4+ T cells and their consequent expression of inflammatory and anti-inflammatory cytokines are altered. In this review, we discuss the mechanisms underlying changes in cytokine release leading to the loss of tolerance and development of autoimmunity.<\/jats:p>","DOI":"10.3390\/v8010005","type":"journal-article","created":{"date-parts":[[2015,12,24]],"date-time":"2015-12-24T10:03:53Z","timestamp":1450951433000},"page":"5","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":99,"title":["HTLV-1, Immune Response and Autoimmunity"],"prefix":"10.3390","volume":"8","author":[{"given":"Juarez","family":"Quaresma","sequence":"first","affiliation":[{"name":"Science Center of Health and Biology. Par\u00e1 State University, Rua Perebebu\u00ed, 2623, Bel\u00e9m, Par\u00e1 66087-670, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gilberto","family":"Yoshikawa","sequence":"additional","affiliation":[{"name":"Science Health Institute, Federal University of Par\u00e1, Pra\u00e7a Camilo Salgado, 1, Bel\u00e9m, Par\u00e1 66055-240, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roberta","family":"Koyama","sequence":"additional","affiliation":[{"name":"Science Center of Health and Biology. Par\u00e1 State University, Rua Perebebu\u00ed, 2623, Bel\u00e9m, Par\u00e1 66087-670, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Dias","sequence":"additional","affiliation":[{"name":"Science Center of Health and Biology. Par\u00e1 State University, Rua Perebebu\u00ed, 2623, Bel\u00e9m, Par\u00e1 66087-670, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Satomi","family":"Fujihara","sequence":"additional","affiliation":[{"name":"Tropical Medicine Center, Federal University of Par\u00e1, Av. General\u00edssimo Deodoro, 92, Bel\u00e9m, Par\u00e1 66055-240, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hellen","family":"Fuzii","sequence":"additional","affiliation":[{"name":"Tropical Medicine Center, Federal University of Par\u00e1, Av. General\u00edssimo Deodoro, 92, Bel\u00e9m, Par\u00e1 66055-240, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2015,12,24]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"151","DOI":"10.1038\/nrmicro754","article-title":"Microorganisms and autoimmunity: Making the barren field fertile?","volume":"1","author":"Fujinami","year":"2003","journal-title":"Nat. Rev. Microbiol."},{"key":"ref_2","first-page":"21","article-title":"Potential triggers of MS. 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