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基于超微结构研究的克罗恩病发病机制假说。

A hypothesis for the pathogenesis of Crohn's disease based on an ultrastructural study.

作者信息

Cook M G, Turnbull G J

出版信息

Virchows Arch A Pathol Anat Histol. 1975;365(4):327-36. doi: 10.1007/BF00471180.

Abstract

The epitheloid cells forming the granulomata of Crohn's disease show striking vacuolation from the coalescing of pinocytotic vesicles with double membrane-bound bodies and their subsequent fusion with lysosomal dense bodies. The fine detail of the granulomata in each individual is uniform but varies from case to case in such a way as to suggest an episodic stimulation of pinocytosis and vacuole formation. The production of such granulomata with these cyclical appearances is consistent with an intermittent stimulus by exogenous antigen or antigen antibody complexes arriving in the diet.

摘要

形成克罗恩病肉芽肿的上皮样细胞呈现出显著的空泡化,这是由于吞饮小泡与双膜结合体合并,随后与溶酶体致密体融合所致。每个个体中肉芽肿的精细结构是一致的,但不同病例之间存在差异,这种差异表明吞饮作用和空泡形成存在间歇性刺激。具有这些周期性表现的此类肉芽肿的产生与饮食中到达的外源性抗原或抗原抗体复合物的间歇性刺激相一致。

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