| First Author | Chai CK | Year | 1976 |
| Journal | Am J Pathol | Volume | 85 |
| Issue | 1 | Pages | 49-72 |
| PubMed ID | 970442 | Mgi Jnum | J:24582 |
| Mgi Id | MGI:72318 | Citation | Chai CK (1976) Reticular cell hyperplasia and amyloidosis in a line of mice with low leukocyte counts. Am J Pathol 85(1):49-72 |
| abstractText | 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 to 6 months, 70% of the mice developed reticular cell hyperplasia in the inguinea lymph nodes, and at 11 to 18 months, about 100% of them developed amyloidosis in the spleen and in the 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. Both intracellular and extracellular amyloid fibrils were found in the liver, spleen, and kidney sections by electron microscopy. 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. In this light, we believe that the pathologic conditions are manifestations of immunologic events that are characteristic of the LLC mice with immune deficiency or abnormality in the immune system. We conclude that the origin of amyloid protein is at the RER. We discuss processes of amyloid fibril formation and some genetic aspects of amyloid development. |
