Toll-like receptor signalling in macrophages links the autophagy pathway to phagocytosis

Areas: Immunology, Signalling

Macrophage toll-like receptor signalling seems to connect phagocytosis and autophagy, two ancient and during evolution highly conserved processes of organism defence against pathogens. In a recent study, Miguel A. Sanjuan and colleagues from the St Jude Children's Research Institute in Memphis (USA) report that a particle that recruits TLRs on murine macrophages on phagocytosis causes the autophagosome marker LC3 to rapidly accumulate in the phagosome. This process is dependent on the autophagy proteins ATG5 and ATG7. Phosphoinositide-3-OH kinase activity and gathering of becelin 1 could be observed.

Autophagy is characterised by the generation of a double-layer membrane, the autophagosome. Fusion with lysosomes enables the autophagosome to destroy its content. This process shares similarities with phagosome maturation. The scientists now translocated becelin 1 and LC3 to the phagosome. The proteins were not involved in the formation of the characteristic double-membrane structures associated with autophagosomes, but they apparently were required for phagosome fusion with lysosomes, leading to a fast acidification and enhanced degeneration of the absorbed organisms.

TLRs activate multiple defence mechanisms within phagocytes, e.g. facilitation of phagosome maturation and autophagy. The scientists therefore consider TLR signalling as a link between both processes, thereby improving the function of common phagosomes.

Related antibodies on antibodies-online.com:

Toll-like Receptors (TLR)

Phosphoinositid-3-Kinase

Phosphoinositide-3-Kinase-γ

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