Intracellular antigens are processed into immunogenic polypeptide fragments as antigenic peptides in the proteasome. membrane shrinkage, facilitate the bacteria invading the cells, and form a vesicle called SCV made up of the bacteria, thereby allowing the long-term survival CD300E of latent bacteria. Evidence suggests that some infections can block the formation of SCV and initiate mitochondrial division and autophagy. Unlike intracellular bacteria, extracellular bacteria cannot invade host cells. For example, mainly relies on the secretion of virulence factors to infect the host and destroy cell structures to activate autophagy. It is still unclear what the molecular mechanism of autophagy induction by extracellular bacterial infection is usually. The exotoxin A (PEA) of the opportunistic pathogen can induce oxidative stress damage in MLE-12 cells and activate autophagy. Vacuolating cytotoxin A (VacA) of (Hp) interferes with endocytic pathways, lysosomal pathways, and host immune responses via cellular vacuolation and induces stress responses. Approximately 30?years ago, the initial evidence suggested that inflammation can induce autophagy. In the last decade, studies have shown that autophagy plays a crucial role in the host defense system against pathogen invasion. The bacteria can be ubiquitinated after invading the cells and degraded through the autophagy pathway. This autophagic process is Bictegravir named xenophagy. Currently, autophagy has been found to be involved in the direct clearance of a variety of pathogens, including (GAS) was the first bacterium found to be cleared by autophagy. GAS infects cells by endocytosis and then forms GAS-containing autophagosome-like vacuoles (GAS-containing autophagic small body-like vesicles) in the cytoplasm. The size of a common autophagosome is usually approximately 1?m. However, the diameter of GcAV can reach 10?m. The formation of GcAV depends on the autophagy core protein complex and the small GTP binding protein RAB7. After fusion of GcAVs with lysosomes to form autophagosomes, GAS is usually degraded and inactivated by lysosomes. GAS is usually inactivated in most cells by the xenophagy pathway explained above. Autophagy maintains intracellular metabolic homeostasis and is closely associated with microbial infections (Gomes and Dikic 2014). On the one hand, research evidence suggests that autophagy is usually involved in the direct clearance of multiple pathogens. On the other hand, parasites have developed ways to circumvent autophagic clearance. When parasites start to proliferate, they rely on the autophagy of the host cells. This evidence suggests that autophagy has dual functions in microbial contamination. Infectious diseases have become progressively severe in recent years. Moreover, new infectious diseases continue to emerge. For example, super bacteria, SARS, Ebola computer virus, avian influenza computer virus, Middle East respiratory syndrome (MERS), and malaria, which have been afflicting people in the tropical regions, bring health threats and severe panic to the public. Antibiotics, interferons, and other medications have had essential functions in combating infectious diseases. However, with antibiotic overuse, bacterial resistance has become a severe problem. Viruses have also been shown to exhibit styles with increasing new mutations and drug resistance. According to WHO reports, the rates of drugs becoming ineffective are currently comparable to the velocity of discovering new drugs. Targeting the intracellular autophagy process has been proven to be an effective way against intracellular contamination. Studies of the molecular mechanisms between autophagy and pathogen-induced signaling pathways will continue to contribute to the discovery of new antibacterial methods with high efficiency and low drug resistance. The Role and Molecular Mechanism of Xenophagy Research has suggested that autophagy plays a key Bictegravir role during the clearance of pathogens such as bacteria and viruses. The host cells identify and obvious the pathogens through Bictegravir autophagic degradation. This is similar to other types of Bictegravir selective autophagy, such as aggregate autophagy (aggrephagy) or mitochondrial autophagy (mitophagy). Autophagy receptors selectively identify ubiquitinated pathogens in xenophagy. After an autophagy receptor interacts with LC3 or GABARAP, the pathogen is usually transported to autophagosomes. Therefore, the clearance of invading pathogens by xenophagy is usually ubiquitination dependent. The modification with ubiquitin provides eat-me signals during xenophagy. can be modified inside.