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Lupus, Vol. 13, No. 5, 372-376 (2004)
DOI: 10.1191/0961203303lu1029oa

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, jdavis{at}medicine.ucsf.edu

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.

Key Words: CTLA4Ig • review • systemic lupus erythematosus


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