PATHOGENESIS OF THE GLOMERULONEPHRITIS OF NZB/W MICE

TLDR

Glomerulonephritis in NZB/W mice develops in association with antinuclear, especially anti‑DNA, antibodies and is marked by granular to lumpy deposition of γG‑ and β1C‑globulins, DNA, and other nuclear antigens along capillary walls and mesangium. Active immunization of young NZB/W mice with DNA‑methylated BSA or injections of soluble DNA boosts antinuclear antibody responses, accelerating and intensifying glomerulonephritis. Elution studies showed that glomerular γG‑globulin is mainly γG2A‑type antibody to soluble nuclear antigens, and soluble DNA injections in mice with anti‑DNA antibodies rapidly accelerate nephritis.

Abstract

The development of glomerulonephritis in NZB/W mice is closely related to the formation of antinuclear, particularly anti-DNA, antibodies. The developing inflammatory glomerular lesions are characterized by the deposition of γG- and ß1C-globulins plus DNA and possibly other nuclear antigens, presumably as complexes, in a granular to lumpy pattern along the capillary walls and in the mesangia. Elution studies revealed the γG-globulin in the glomeruli to be largely γG2A-type antibody to soluble nuclear antigens. Enhancement of the antinuclear antibody response by active immunization of young NZB/W mice with DNA-methylated BSA hastens the development and increases the severity of the glomerulonephritis. Similarly, injections of soluble DNA into NZB/W mice with circulating anti-DNA antibodies but with as yet little nephritis causes rapid progression of nephritis.