{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,9,30]],"date-time":"2024-09-30T04:18:29Z","timestamp":1727669909723},"reference-count":48,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2001,5,1]],"date-time":"2001-05-01T00:00:00Z","timestamp":988675200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Critical Reviews in Oral Biology &amp; Medicine"],"published-print":{"date-parts":[[2001,5]]},"abstract":"<jats:p> The study of pathogenetic factors in Sjogren's syndrome [SS] has been problematic, given the overall paucity of coherent data that integrate basic research with clinical findings. The presumed autoimmune nature of SS suggests T-cells, autoantibodies, and cytokines as possible immune factors in the initiation and progression of SS. Recent work on programmed cell death (apoptosis) in SS and its models suggests this as a fourth potential mechanism of disease. These four areas of SS research are reviewed with an emphasis on the most recent findings related to mechanisms of disease. New findings confirm the potential for antigen presentation to T-cells in the salivary glands, as well as involvement of other adhesion molecules with respect to T-cell functions. Restrictions on the receptor repertoires of infiltrating T-cells are discussed, as are new findings on antigenic specificities of these cells. New findings on the specificities of autoantibodies observed in SS are reviewed with an eye toward potential mechanisms for depression of exocrine secretory capacity. Stimulating new findings concerning cytokine production in salivary and lacrimal gland are noted. Particular points of interest with regard to apoptosis include the wide range of values obtained for apoptotic activity in SS and its models, and potential means of resolving discongruent results and the study of factors influencing apoptosis are discussed. <\/jats:p>","DOI":"10.1177\/10454411010120030301","type":"journal-article","created":{"date-parts":[[2009,1,9]],"date-time":"2009-01-09T00:40:32Z","timestamp":1231461632000},"page":"244-251","source":"Crossref","is-referenced-by-count":9,"title":["Pathogenetic Factors in Sj\u00f6gren's Syndrome: Recent Developments"],"prefix":"10.1177","volume":"12","author":[{"given":"T.R.","family":"Esch","sequence":"first","affiliation":[{"name":"Department of Immunology, Forsyth Institute, 140 Fenway, Harvard-Forsyth Department of Oral Biology, Harvard School of Dental Medicine, Boston, MA 02115,"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2001,5,1]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1093\/rheumatology\/37.2.179"},{"key":"atypb2","unstructured":"Bacman S., Perez LC, Sterin-Borda L., Hubscher O., Arana R., Borda E. (1998a). Autoantibodies against lacrimal gland M3 muscarinic acetylcholine receptors in patients with primary Sjogren's syndrome. 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Preferential localization of CD8+ alpha E beta 7+ T cells around acinar epithelial cells with apoptosis in patients with Sjogren's syndrome. J Immunol 163:2226-2235.","DOI":"10.4049\/jimmunol.163.4.2226"},{"key":"atypb13","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4400414"},{"key":"atypb14","doi-asserted-by":"publisher","DOI":"10.1002\/1529-0131(199902)42:2<240::AID-ANR5>3.0.CO;2-I"},{"key":"atypb15","doi-asserted-by":"crossref","unstructured":"Grasl-Kraupp B., Ruttkay-Nedecky B., Koudelka H., Bukowska K., Bursch W., Schulte-Hermann R. (1995). In situ detection of fragmented DNA (TUNEL assay) fails to discriminate among apoptosis, necrosis, and autolytic cell death: a cautionary note. Hepatology 21:1465-1468.","DOI":"10.1002\/hep.1840210534"},{"key":"atypb16","unstructured":"Grisius MM, Bermudez DK, Fox PC (1997). Salivary and serum interleukin 6 in primary Sjogren's syndrome. 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