CTLA4Ig: a novel inhibitor of costimulation

  • M Dall’Era
    Division of Rheumatology, University of California San Francisco, San Francisco, USA
  • J Davis
    Division of Rheumatology, University of California San Francisco, San Francisco, USA,

書誌事項

公開日
2004-05
権利情報
  • https://journals.sagepub.com/page/policies/text-and-data-mining-license
DOI
  • 10.1191/0961203303lu1029oa
公開者
SAGE Publications

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説明

<jats:p> T cell costimulatory pathways are believed to play important roles in the pathogenesis of various autoimmune diseases including systemic lupus erythematosus(SLE). Animal models of SLE support the role of T cell costimulation in B cell activation and the production of autoantibodies. CTLA4Ig is a novel fusion protein that interferes with T cell costimulation by inhibiting the CD28-B7 interaction. A pivotal study demonstrated the ability of CTLA4Ig to suppress the production of anti-dsDNA antibodies and decrease nephritisin lupus prone mice. In an additionalstudy, the combination of CTLA4Ig and cyclophosphamidesignificantly reduced proteinuria and prolonged survival in mice with advanced nephritis. In small human studies of psoriasis and rheumatoid arthritis, CTLA4Ig improved clinical outcomes and was well tolerated. These promising experienceswith CTLA4Ig have paved the way for future studies in human SLE. </jats:p>

収録刊行物

  • Lupus

    Lupus 13 (5), 372-376, 2004-05

    SAGE Publications

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