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Lupus
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Block and tackle: CTLA4Ig takes on lupus

A Davidson

Departments of Medicine and Microbiology, Columbia University, New York, NY, USA, ad2247{at}columbia.edu

B Diamond

Departments of Medicine and Microbiology, Columbia University, New York, NY, USA

D Wofsy

Department of Veterans Affairs Medical Center and the University of California, San Francisco, CA, USA

D Daikh

Department of Veterans Affairs Medical Center and the University of California, San Francisco, CA, USA

Blockade of antigen nonspecific costimulatory signals is a promising approach for the treatment of autoimmune diseases including systemic lupus erythematosus (SLE). CTLA4Ig, an antagonist of the CD28/B7 costimulatory interaction, effectively prevents SLE onset in several murine models and, when used in combination with cyclophosphamide, can induce remission of active SLE nephritis. In this review we describe the known mechanisms of action of CTLA4Ig both in normal immunity and in autoimmune disease models and address issues about its activity that still need to be resolved. We discuss the preclinical use of CTLA4Ig in murine SLE models and the rationale for a clinical trial in SLE patients.

Key Words: B cells • costimulation • CTLA4Ig • lymphocyte activation • SLE • T cells

Lupus, Vol. 14, No. 3, 197-203 (2005)
DOI: 10.1191/0961203305lu2136oa
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