LAP: the protector against autoimmunity

Abstract

The autophagy-related process LC3-Associated Phagocytosis, or LAP, is known to control the degradation of engulfed cells and microorganisms. Now Martinez et al. discover that LAP controls immune responses to dying cells and its inhibition leads to development of Systemic Lupus Erythematosus-like disease.

Figure 1

Dying cell clearance involves phagocytic engulfment (left side) and corpse degradation (right side). Degradation is regulated by autophagy proteins that lipidate LC3 (green circles) onto phagosomes, forming an LC3-Associated Phagosome or LAPosome. LAPosome formation requires LC3 lipidation machinery, as well as Rubicon and Nox2 (green text), but not the ULK complex or ATG14 (red text). The inhibition of LAPosome formation blocks corpse degradation and leads to Systemic Lupus Erythematosus (SLE)-like disease in mice (right, blue box).