| Literature DB >> 4924198 |
R C Mellors, T Shirai, T Aoki, R J Huebner, K Krawczynski.
Abstract
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.Entities:
Mesh：
Year: 1971 PMID： 4924198 PMCID： PMC2138888 DOI： 10.1084/jem.133.1.113
Source DB: PubMed Journal: J Exp Med ISSN： 0022-1007 Impact factor: 14.307