Hijacked phagosomes and leukocyte activation: an intimate relationship.

J Leukoc Biol

URMITE CNRS UMR 6236-IRD 3R198, Institut Fédératif de Recherche 48, Université de la Méditerranée, Marseille, France.

Published: March 2011

AI Article Synopsis

  • Intracellular pathogens use various strategies to survive inside host cells, such as manipulating the formation of phagolysosomes to create their own replicative vacuoles.
  • Although research has explored how naive leukocytes respond, the impact of cytokine-induced leukocyte activation on phagosome biogenesis remains under-examined.
  • This review discusses how cytokines influence endocytosis and phagosome formation, particularly focusing on the mechanisms utilized by pathogens like Coxiella burnetii and Mycobacterium tuberculosis to exploit these processes.

Article Abstract

Intracellular pathogens have developed different strategies to survive within host cells. For example, these pathogens might interfere with the biogenesis of phagolysosomes, thereby forming replicative vacuoles. Although the complex mechanisms used by pathogens to hijack the biogenesis of phagolysosomes have been elucidated in naive leukocytes, the role of leukocyte activation in this process has not yet been investigated. Leukocytes are known to be activated by cytokines, and several reports have demonstrated that several cytokines modulate the endocytic pathway and thereby, affect phagosome biogenesis. These observations provide molecular evidence that endocytosis can be regulated by the immune environment. In this review, we highlight the effect of leukocyte activation by cytokines on the endocytic pathway and on phagosome biogenesis. We briefly describe the mechanism of phagolysosome formation before focusing on the strategies used by two bacterial pathogens, Coxiella burnetii and Mycobacterium tuberculosis, to hijack phagolysosome biogenesis. Finally, we emphasize the effect of leukocyte activation on the endocytic pathway and on phagolysosome formation, which has not been highlighted to date.

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http://dx.doi.org/10.1189/jlb.0510270DOI Listing

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