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. 1980;62(3):241-54.
doi: 10.1007/BF00926565.

Pathogenesis and host response in subcutaneous alveolar hydatidosis. I. Histogenesis of alveolar cyst and a qualitative analysis of the inflammatory infiltrates

Pathogenesis and host response in subcutaneous alveolar hydatidosis. I. Histogenesis of alveolar cyst and a qualitative analysis of the inflammatory infiltrates

Z Ali-Khan et al. Z Parasitenkd. 1980.

Abstract

C57L/J male mice were infected subcutaneously in their left flank with 10 cysts of Echinococcus multilocularis. The dimensions and histologic features of the larval cyst mass (LCM) were determined at three days, at weekly intervals for 12 weeks, and at 22 weeks postinfection. The LCM doubled its size between 3 and 12 weeks, and at 22 weeks it was five times larger than at three weeks. During the proliferative phase, the LCM was infiltrated massively by neutrophils, macrophages, and progenitors of the plasma cell series. The first two cell types were found firmly bound to the laminated layer of both intact and degenerating cysts, whereas plasma cells colonized the fibrohistocytic corona and the interlacunar stroma harboring individual cysts. By 22 weeks, the proliferation of the cysts had ceased and histologically the LCM consisted of fibrous and fibrohistiocytic stroma, thick-walled fertile and sterile brood capsules, and predominantly plasmacytic and histiocytic infiltrates. In addition to exogenous budding evidence has been presented also suggesting the role of free germinal cells in the histogenesis of LCM. Regulation of cyst proliferation in susceptible hosts is discussed with reference to antibody-dependent cell mediated cytotoxicity with nonlymphoid inflammatory cells.

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