Renal disease in (NZB x NZW) F1 mice treated with antilymphocytic antibody. II. Effects of restoration with isogeneic, allogeneic, and xenogeneic lymphoid cells.
Intensive treatment of 2-month old (NZB×NZW) F1 hybrid (BW) mice with antilymphocytic IgG (ALG) induced immediate renal disease, even when the mice were tolerant to rabbit IgG (NRG). Many of the features of the natural renal disease were present including glomerular hypercellularity with capillary narrowing and perivascular cellular infiltrates, but there was usually little evidence of immune complex deposition or of glomerular basement membrane (GBM) thickening as seen on immune fluorescence and electron microscopy, respectively. The induction of acute renal disease was prevented by syngeneic or allogeneic cell transfer, or by azathioprine. While moderate doses of ALG may suppress the onset of renal disease in mice tolerant to NRG, it is suggested that excessive lymphocyte depletion encourages the proliferation of lymphoid cells and reticulum cells which are resistant to ALG treatment, but not to azothioprine, and may be under viral influence. Re-establishment of control over this process would account for the effectiveness of a graft of syngeneic, allogeneic or xenogeneic spleen, thymus and bone marrow cells.