| First Author | Cathcart ES | Year | 1996 |
| Journal | Amyloid | Volume | 3 |
| Issue | 2 | Pages | 119-123 |
| Mgi Jnum | J:34709 | Mgi Id | MGI:82164 |
| Doi | 10.3109/13506129609014363 | Citation | Cathcart ES, et al. (1996) Macrophage function in azocasein-induced amyloidosis in CBA/J and A/J mice. Amyloid 3(2):119-123 |
| abstractText | It is known that a single gene governs resistance to amyloidosis induced by azocasein in A/J compared to CBA/J mice. We wished to determine whether this trait might he linked to differences in macrophage activation as measured by Fc gamma-receptor (Fc gamma-R) and C3b receptor (C3b-R) phagocytosis of sheep erythrocytcs and/or TNF secretion by adherent resident peritoneal cells. Macrophages from preamyloidotic and amyloidotic CBA/J mice showed marked enhancement of Fc gamma-R and C3h-R binding activity. Macrophages from A/J mice receiving multiple azocasein injections showed a significant increase in Fc gamma-R but not in C3b-R phagocytic indices. Adherent peritoneal cells from control and azocasein-treated AN mice produced higher TNF levels than control and azocasein-treated CBA/J mice. In both strains, peritoneal macrophage TNF secretion was depressed after 10 azocasein injections. Our findings differ from previous studies in which the amyloid deposition phase was associated with normal or depressed phagocytosis. On the other hand, down-regulation of TNF production by macrophages from amyloidotic CBA/J mice and preamyloidotic A/J mice suggests that this cytokine may play an important role in the pathogenesis of experimentally induced amyloidosis. |
