The Journal of Experimental Medicine
Cytokines Montreal 2008
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The Journal of Experimental Medicine, Vol 133, 113-132, Copyright © 1971 by The Rockefeller University Press

ARTICLE

WILD-TYPE GROSS LEUKEMIA VIRUS AND THE PATHOGENESIS OF THE GLOMERULONEPHRITIS OF NEW ZEALAND MICE

Robert C. Mellors M.D.1, Toshikazu Shirai M.D.1, Tadao Aoki M.D.1, Robert J. Huebner M.D.1, and Krzysztof Krawczynski M.D.1

1 From The Hospital for Special Surgery—Philip D. Wilson Research Foundation, affiliated with The New York Hospital—Cornell University Medical College, and the Department of Pathology, Cornell University Medical College, New York, 10021, the Division of Immunology, Sloan-Kettering Institute for Cancer Research, New York 10021, and the Viral Carcinogenesis Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

The pathogenesis of the spontaneous glomerulonephritis of NZB and (NZB x NZW) F1 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) F1 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) F1 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) F1 hybrid mice, both in the mesangium as observed in NZB mice and also in the wall of the peripheral capillary loops of the glomeruli.

Submitted on August 12, 1970


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