Treatment of human cit-fibrinogen-immunized DR4 Tg mice with CTLA-4Ig fusion protein, a soluble form of the CTLA-4 receptor which inhibits T cell activation by competing with CD28 for binding to the costimulatory ligand CD80/CD86 (174), restrained the activation of cit-fibrinogen-specific T cell responses, and halted the progression of arthritis (152). The gene discussed is CIT; the disease is arthritic joint disease.