Renal disease in (NZB x NZW)F1 hybrid mice treated with anti-lymphocytic antibody.

Anti-lymphocytic IgG (ALG) in moderate doses postponed the onset of spontaneous renal disease in (NZB × NZW)F hybrid (BW) mice decreasing their mortality. This result only occurred if antibody formation to the ALG was prevented by first rendering the mice tolerant to normal rabbit IgG (NRG), otherwise acceleration of renal disease occurred. This acceleration was particularly marked if γ-globulin, rather than a purified IgG preparation of ALG were used and was further enhanced by adult thymectomy. The development of antinuclear antibody was not delayed by ALG nor was the rise in the serum IgM levels. The effects of ALG are seriously modified by alterations in factors such as dosage used, preceding tolerance to the NRG, thymectomy and strain of mouse used.