New concepts in the pathogenesis of primary and secondary amyloid disease.
Despite the marked progress obtained in the structural and amino acid sequencing data of amyloid proteins our understanding of the cellular mechanisms causing the deposition of amyloid fibrils is still poor. Some of the questions about the cellular events leading to the synthesis of amyloid fibrils can be approached by evaluating the immune reactivity of animals that develop amyloid after repeated daily casein injections. Recent studies carried out in a mouse model indicate that macrophage activation associated with T-cell suppression and followed by B-cell proliferation appear to be responsible for the immunopathological abnormalities in both primary and secondary amyloid disease.
D000686:Amyloidosis / Q000209:etiology / Q000276:immunology*; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D002364:Caseins; D004195:Disease Models, Animal; D006801:Humans; D007165:Immunosuppression Therapy; D008264:Macrophages / Q000276:immunology; D051379:Mice; D009101:Multiple Myeloma / Q000276:immunology; D009374:Neoplasms, Experimental / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D002364:Caseins