RETICULAR CELL HYPERPLASIA AND AMYLOIDOSIS IN A LINE OF MICE WITH LOW LEUKOCYTE COUNTS

  • 1 January 1976
    • journal article
    • research article
    • Vol. 85  (1) , 49-72
Abstract
Two pathologic conditions, reticular cell hyperplasia and amyloidosis, were studied in a strain of mice selectively bred for low leukocyte counts (LLC). At the age of 3-6 mo., 70% of the mice developed reticular cell hyperplasia in the inguinal lymph nodes; at 11-18 mo., about 100% of them developed amyloidosis in the spleen, kidney, liver and adrenal glands. Immunofluorescence was revealed in the glomeruli, interstitium of the tubules and the amyloid skeleton of the papilla when the kidney sections were incubated with fluorescein-labeled antimouse immunoglobulins. Intracellular and extracellular amyloid fibrils were found in the liver, spleen and kidney sections by EM. Distended rough endoplasmic reticulum (RER) cisternae and hypertrophy of RER with or without the simultaneous presence of amyloid fibrils in the reticular cells of the spleen and Kupffer cells of the liver were observed. The pathologic conditions are apparently manifestations of immunologic events that are characteristic of the LLC mice with immune deficiency or abnormality in the immune system. The origin of amyloid protein is at the RER. Processes of amyloid fibril formation and some genetic aspects of amyloid development are discussed.