巨噬细胞在麻风病发病中的作用

Rhana Berto da Silva Prata, M. G. M. Barbosa, B. Silva, Jéssica Araújo da Paixão de Oliveira, Tamiris Lameira Bittencourt, R. Pinheiro
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引用次数: 6

摘要

麻风病是一种由细胞内病原体麻风分枝杆菌引起的慢性传染病。该病可根据宿主的免疫状态表现出不同的临床形式。麻风分枝杆菌可能感染巨噬细胞和雪旺细胞,最近的研究表明,巨噬细胞是决定疾病结局的基础细胞。少杆菌型患者的皮肤病变以促炎表型(M1)的巨噬细胞为主,而多杆菌型患者的皮肤病变以抗炎表型(M2)的巨噬细胞为主。最近,研究表明,自噬负责控制少杆菌巨噬细胞中的细菌负荷,自噬的阻断参与了多杆菌细胞急性炎症反应发作的发生。因此,旨在诱导感染巨噬细胞自噬的策略不仅有望提高多药治疗(MDT)的疗效,而且有望避免导致麻风患者残疾的反应性事件的发生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Macrophages in the Pathogenesis of Leprosy
Leprosy is a chronic infectious disease caused by the intracellular pathogen Mycobacterium leprae . The disease may present different clinical forms depending on the immunological status of the host. M. leprae may infect macrophages and Schwann cells, and recent studies have demonstrated that macrophages are funda-mental cells for determining the outcome of the disease. Skin lesions from patients with the paucibacillary form of the disease present a predominance of macrophages with a pro-inflammatory phenotype (M1), whereas skin lesions of multibacillary patients present a predominance of anti-inflammatory macrophages (M2). More recently, it was shown that autophagy is responsible for the control of bacillary load in paucibacillary macrophages and that the blockade of autophagy is involved in the onset of acute inflammatory reactional episodes in multibacillary cells. So, strategies that aim to induce autophagy in infected macrophages are promising not only to improve the efficacy of multidrug therapy (MDT) but also to avoid the occurrence of reactional episodes that are responsible for the disabilities observed in leprosy patients.
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