Wild-type Gross leukemia virus and the pathogenesis of the glomerulonephritis of New Zealand mice.
The pathogenesis of the spontaneous glomerulonephritis of NZB and (NZB x NZW) F(1) hybrid mice is related at least in part to the formation of natural antibody against antigens of the G (Gross) system, and apparently to the deposition in the glomeruli of immune complexes of G natural antibody with G soluble antigen (GSA), type-specific antigen specified by wild-type Gross leukemia virus. G natural antibody and GSA are detectable in the acid-buffer eluate of the kidneys of NZB mice during the course of the glomerulonephritis. (NZB x NZW) F(1) hybrid mice develop glomerulonephritis and produce GSA and free G natural antibody earlier in life than do NZB mice. The proteinuria manifestation of the gomerulonephritis of (NZB x NZW) F(1) hybrid mice becomes increasingly prevalent as GSA undergoes immune elimination from the circulation. Gross leukemia virus-specified antigens together with bound immunoglobulins are located in the glomerular lesions of (NZB x NZW) F(1) hybrid mice, both in the mesangium as observed in NZB mice and also in the wall of the peripheral capillary loops of the glomeruli.
D000406:AKR murine leukemia virus / Q000276:immunology / Q000472:pathogenicity*; D000818:Animals; D000917:Antibody Formation; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000209:etiology* / Q000276:immunology / Q000662:veterinary; D006967:Hypersensitivity / Q000662:veterinary*; D051379:Mice; D012376:Rodent Diseases / Q000276:immunology*