Disappearance and reappearance of B cells after in vivo treatment with monoclonal anti-I-A antibodies.

Previous studies have shown that treatment with antibodies to the murine I-A antigen encoded in the major histocompatibility complex attenuates experimental allergic encephalitis and experimental autoimmune myasthenia gravis. These studies were conducted with SJL mice, an inbred strain that is highly susceptible to the induction of these diseases. Here we show that injection of monoclonal anti-I-A antibody in the amounts used for the above studies rapidly depletes B cells. Fluorescence-activated cell sorter (FACS) multiparameter analysis of the B-cell subpopulations in treated animals shows that maximum depletion occurs around 5 days after treatment and that recovery of some subpopulations i still incomplete 1 month later. SJL mice are more sensitive to this B-cell depletion and recover more slowly than putatively normal C3H.Ighb (CKB) mice. Some components of the primary, secondary and tertiary IgG antibody responses are reduced in anti-I-A-treated SJL animals immunized after the first and second anti-I-A injections. The persistence of some antibody response impairment well beyond the time when anti-I-A disappears raises a note of caution concerning human therapy protocols based on the injection of anti-Ia antibodies.