{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T13:44:00Z","timestamp":1790516640410,"version":"4.1.0"},"reference-count":119,"publisher":"MDPI AG","issue":"1","license":[{"start":{"date-parts":[[2022,1,6]],"date-time":"2022-01-06T00:00:00Z","timestamp":1641427200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001691","name":"KAKENHI","doi-asserted-by":"publisher","award":["JP19K08884"],"award-info":[{"award-number":["JP19K08884"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Viruses"],"abstract":"<jats:p>Viruses are a possible cause for Sj\u00f6gren\u2019s syndrome (SS) as an environmental factor related to SS onset, which exhibits exocrine gland dysfunction and the emergence of autoantibodies. Although retroviruses may exhibit lymphocytic infiltration into exocrine glands, human T-cell leukemia virus type 1 (HTLV-1) has been postulated to be a causative agent for SS. Transgenic mice with HTLV-1 genes showed sialadenitis resembling SS, but their phenotypic symptoms differed based on the adopted region of HTLV-1 genes. The dominance of tax gene differed in labial salivary glands (LSGs) of SS patients with HTLV 1-associated myelopathy (HAM) and adult T-cell leukemia. Although HTLV-1 was transmitted to salivary gland epithelial cells (SGECs) by a biofilm-like structure, no viral synapse formation was observed. After infection to SGECs derived from SS patients, adhesion molecules and migration factors were time-dependently released from infected SGECs. The frequency of the appearance of autoantibodies including anti-Ro\/SS-A, La\/SS-B antibodies in SS patients complicated with HAM is unknown; the observation of less frequent ectopic germinal center formation in HTLV-1-seropositive SS patients was a breakthrough. In addition, HTLV-1 infected cells inhibited B-lymphocyte activating factor or C-X-C motif chemokine 13 through direct contact with established follicular dendritic cell-like cells. These findings show that HTLV-1 is directly involved in the pathogenesis of SS.<\/jats:p>","DOI":"10.3390\/v14010100","type":"journal-article","created":{"date-parts":[[2022,1,9]],"date-time":"2022-01-09T23:35:09Z","timestamp":1641771309000},"page":"100","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Does HTLV-1 Infection Show Phenotypes Found in Sj\u00f6gren\u2019s Syndrome?"],"prefix":"10.3390","volume":"14","author":[{"given":"Hideki","family":"Nakamura","sequence":"first","affiliation":[{"name":"Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masako","family":"Tsukamoto","sequence":"additional","affiliation":[{"name":"Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yosuke","family":"Nagasawa","sequence":"additional","affiliation":[{"name":"Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noboru","family":"Kitamura","sequence":"additional","affiliation":[{"name":"Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0036-2039","authenticated-orcid":false,"given":"Toshimasa","family":"Shimizu","sequence":"additional","affiliation":[{"name":"Division of Advanced Preventive Medical Sciences, Department of Immunology and Rheumatology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8501, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Atsushi","family":"Kawakami","sequence":"additional","affiliation":[{"name":"Division of Advanced Preventive Medical Sciences, Department of Immunology and Rheumatology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8501, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kinya","family":"Nagata","sequence":"additional","affiliation":[{"name":"Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5791-3359","authenticated-orcid":false,"given":"Masami","family":"Takei","sequence":"additional","affiliation":[{"name":"Division of Hematology and Rheumatology, Department of Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2022,1,6]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"769","DOI":"10.1136\/ard.51.6.769","article-title":"Antibodies to HTLV-I in Sjogren\u2019s syndrome","volume":"51","author":"Eguchi","year":"1992","journal-title":"Ann. 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