Journal
LUPUS
Volume 14, Issue 3, Pages 197-203Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1191/0961203305lu2136oa
Keywords
B cells; costimulation; CTLA4Ig; lymphocyte activation; SLE; T cells
Categories
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available