Monoclonal antibodies to TNF-α, IFN-γ, IL-12, CD40L, inducible co-stimulator (ICOS), and cytotoxic T-lymphocyte antigen 4 immunoglobulin (CTLA-4Ig) were used to block TNF-α and IFN-γ production, examine clinical index in mice with GPI-induced arthritis, and determine anti-GPI antibody production. This evidence concerns the gene GPI and arthritic joint disease.