Abstract
The establishment of parasitic infection is dependent on the development of efficient strategies to evade the host defense mechanisms. Phosphatidylserine (PS) molecules are pivotal for apoptotic cell recognition and clearance by professional phagocytes. Moreover, PS receptors are able to trigger anti-inflammatory and immunosuppressive responses by phagocytes, either by coupled enzymes or through the induction of regulatory cytokine secretion. These PS-dependent events are exploited by parasites in a mechanism called apoptotic mimicry. Generally, apoptotic mimicry refers to the effects of PS recognition for the initiation and maintenance of pathogenic infections. However, in this context, PS molecules can be recognized on the surface of the infectious agent or in the surface of apoptotic host debris, leading to the respective denomination of classical and non-classical apoptotic mimicry. In this review, we discuss the role of PS in the pathogenesis of several human infections caused by protozoan parasites.DHtcwtNhUSewf3HGLcBbyTVideo
Highlights
Apoptosis and apoptotic mimicry Parasites have to cope with the host immune system to establish infection
In this review we propose to discuss the role of PS in the context of both classical and non-classical apoptotic mimicry, on the perspective of different parasite infections of interest for human health
We have recently shown that the mechanism of inhibition of nitric oxide (NO) production differs in distinct macrophage cell lines: Inducible nitric oxide synthase (iNOS) is degraded in peritoneal macrophage-like lineage but remains expressed in RAW 264.7 lineage [52]
Summary
Apoptosis and apoptotic mimicry Parasites have to cope with the host immune system to establish infection. * Correspondence: lmwjoao@macae.ufrj.br 1Laboratório de Imunoparasitologia, Campus UFRJ Macaé, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil Full list of author information is available at the end of the article able to expose phosphatidylserine (PS) in the outer leaflet of the plasma membrane, and that this molecule is important for amastigote infection and maintenance of the consequent experimental leishmanial disease [5].
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