Autophagy is critical for group 2 innate lymphoid cell metabolic homeostasis and effector function复制标题

自噬对第2组固有淋巴细胞代谢稳态和效应细胞功能至关重要

Macroautophagy (hereafter referred to as autophagy) is the intracellular process by which damaged organelles are cleared and recycled, playing a critical role for cell survival. Defects in autophagy result in accumulation of damaged organelles such as mitochondria with the potential release of reactive oxygen species (ROS) that can affect apoptosis. This can in turn lead to activation of the immune system and the development of inflammatory diseases. Aside from bulk degradation, autophagy also plays a pivotal role in the regulation of metabolites levels including glucose and fatty acids (FA) and the balance of energy-generating metabolic pathways in different immune cell populations by modulating fuel dependency. Given that immune activation is highly energy dependent and requires specific type of fuel, the mechanisms by which immune cells obtain their energy offers a new platform to modify immune functions. Unlike activated T helpers cells that favor glycolytic metabolism, memory and regulatory T cells are mainly fueled using mitochondrial oxidative phosphorylation (OXPHOS). Similarly, innate lymphoid cells have also been shown to predominantly generate energy by fatty acid oxidation. Although, it has been demonstrated that autophagy plays an important role in the development of innate lymphoid cells, further studies are required to understand how modulation of autophagy and metabolic balance affect homeostasis and effector functions of ILC2 in the context of diseases associated with ILC2s.

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