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pubmed-article:8513590pubmed:abstractTextRheumatoid arthritis is an autoimmune disease which is characterized by chronic polyarthritis and joint destruction as well as by extra-articular manifestations, typically including the appearance of rheumatoid nodules. Although the pathogenesis of the disease is unknown, substantial evidence suggests that it is T cell-mediated. In contrast to experimental models, the disease-mediating T cells in the human situation have never been isolated or identified. We expanded T lymphocytes from human rheumatoid nodules by IL-2 stimulation and observed a marked oligoclonality among these expanded lymphocytes. This tendency towards oligoclonality was not seen in IL-2-expanded lymphocytes from peripheral blood. We hypothesize that this oligoclonal expansion reflects a clonally restricted in situ preactivation of lymphocytes and that precisely these preactivated cells are involved in the pathogenesis of the rheumatic process.lld:pubmed
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pubmed-article:8513590pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:8513590pubmed:articleTitleT cell receptor V beta usage in rheumatoid nodules: marked oligoclonality among IL-2 expanded lymphocytes.lld:pubmed
pubmed-article:8513590pubmed:affiliationDepartment of Rheumatology, University Hospital, Ghent, Belgium.lld:pubmed
pubmed-article:8513590pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8513590pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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