Immune Signaling and Autophagy Regulation

Abstract

Autophagy is one of the key degradation systems in organisms. Starvation and nutrient deprivation induce autophagy activation, providing energy and anabolic substances to maintain energy homeostasis. A variety of signals participate in the induction of autophagy, including endoplasmic reticulum stress, oxidative stress, and activation of immune signals. Autophagy is closely related to immunity and inflammation. Autophagy-related gene mutations increase the risk of infectious diseases and malignancies. Autophagy can be regarded as an effector of the immune system to eliminate invading pathogens and is also involved in the immune system recognizing the invasion of pathogens. Autophagy plays important roles in regulating innate immunity and adaptive immunity. In terms of innate immunity, autophagy not only participates in the clearance of pathogens and cell debris after apoptosis but also plays a protective role against toxins, regulates cytokine production, and activates the inflammasome. In the adaptive immune response, autophagy plays an important regulatory role in thymic selection, T cell maturation, T cell polarization, T cell and B cell homeostasis, antigen processing, antigen presentation, and antibody response. On the other hand, autophagy is regulated by immunological and stress signals. The crosstalk between these signaling pathways helps maintain homeostasis and physiological functions. Dysfunction of these regulatory networks is the cause of several kinds of diseases.