期刊
LUPUS
卷 14, 期 3, 页码 197-203出版社
SAGE PUBLICATIONS LTD
DOI: 10.1191/0961203305lu2136oa
关键词
B cells; costimulation; CTLA4Ig; lymphocyte activation; SLE; T cells
类别
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.
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