Scheinberg M A, Cathcart E S
Clin Exp Immunol. 1978 Jul;33(1):185-90.
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.
尽管在淀粉样蛋白的结构和氨基酸测序数据方面取得了显著进展，但我们对导致淀粉样原纤维沉积的细胞机制的了解仍然有限。关于导致淀粉样原纤维合成的细胞事件的一些问题，可以通过评估在每天重复注射酪蛋白后发生淀粉样变的动物的免疫反应性来解决。最近在小鼠模型中进行的研究表明，与T细胞抑制相关并随后伴有B细胞增殖的巨噬细胞激活，似乎是原发性和继发性淀粉样疾病免疫病理异常的原因。
