Few studies proved that deletion of mutation of IFN-γ in the B6 IFN-γ-KO CIA model highlighted the pathogenic role of B cells in arthritis development; CBA/N xid43 mice (defective B cell development by X-linked immunodeficiency) and muMT mice (depletion of B cells by deletion of the IgM heavy chain gene) did not produce antibody response at the time of CII immunization; they were therefore resistant to CIA induction [86,96]. This evidence concerns the gene IFNG and arthritic joint disease.