KFU. Card publication. Аутофагия и LC3-ассоциированный фагоцитоз: сходства и различия (Обзор)

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АУТОФАГИЯ И LC3-АССОЦИИРОВАННЫЙ ФАГОЦИТОЗ: СХОДСТВА И РАЗЛИЧИЯ (ОБЗОР)

Form of presentation

Articles in Russian journals and collections

Year of publication

2023

Язык

русский

Authors, employees of KFU

Ibragimov Bulat Ramilevich, author

Skibo Yuliya Valerevna, author

Bibliographic description in the original language

Ibragimov B.R. Autofagiya i LC3-associirovannyy fagocitoz: skhodstva i razlichiya (Obzor)/ B.R. Ibragimov, Yu.V Skibo, Z.I. Abramova //Medicinskaya immunologiya. -2023, T. 25, № 2, str. 233-252(Medical Immunology (Russia)/ Meditsinskaya Immunologiya) DOI: 10.15789/1563-0625-AAL-2569.

Annotation

Abstract. Previously, autophagy was termed as a mechanism used by the cells with a lack of essential nutrients supporting homeostasis. Over the decade of studies, autophagy proved to be a more complex, ambiguous mechanism. Its activation depends on the nature of stimulus, type of immune cells and the final result. Both canonical and non-canonical autophagy, being similar in molecular events, but showing their own distinctive features, are key processes in protecting the body from penetration of intracellular pathogens, maintaining the required level of nutrients in the cell, and removing damaged organelles and cells. Canonical autophagy probably evolved as a homeostatic response to cellular stress and nutritional deficiencies, whereas non-canonical autophagy emerged as a response to suppression of inflammation. Non-canonical autophagy, hereinafter referred to as LC3-associated phagocytosis (LAP), combines the molecular mechanism of phagocytosis with an autophagy mechanism characterized by ingestion of exogenous pathogens, formation of phagosomes (laposomes) and enhanced fusion with lysosomes, followed by degradation of their contents. Significant differences were found between the processes of LAP- and canonical autophagy, which are similar in its mechanism of action. The presence of PI3K complexes in both processes, utilization and intracellular degradation of the “cargo” which is not required for the cells and organism proceeding in the lysosomes, and involvement of almost the same proteins provide similarity of their mechanisms. However, there are differences in the initiation of the processes, e.g., different types of PI3K complexes (in autophagy, PI3K III class 1 and 2 types; in LAP PI3K III, class 3 type), usage of reactive oxygen species in LAP, different types of regulatory proteins involved (ULK1, FIP200, ATG13 , Ambra1, WIPI2, ATG14 in autophagy; and Rubicon and NOX2 in LC3-associated phagocytosis), different number of layers in the membrane structure in which lysis occurs (double-membrane autophagolysosome and single-layer membrane in laposomes) clearly depict the variety of canonical and non-canonical autophagy. The two pathways are directed for different types of biological objects, i.e., intracellular pathogens, dysfunctional proteins and organelles in autophagy, and extracellular pathogens, apoptotic bodies, bacteria, utilized in LAP, thus making these mechanisms completely different in their significance. Collectively, the new data indicate that autophagy performed via both canonical and non-canonical pathways, has evolved into a host defense mechanism capable of resisting immunological and pathogenic stress and mediating immunological tolerance to both intra- and extracellular threats. The present review discusses fundamental molecular differences between these mechanisms, as well as their role in immunity, based on the latest literature data.

Keywords

аутофагия, LC3-ассоциированный фагоцитоз, LC3, Beclin-1, Vps34, аутоиммунитет, воспаление

The name of the journal

Медицинская иммунология

URL

https://www.mimmun.ru/mimmun/article/view/2569/1640

Please use this ID to quote from or refer to the card

https://repository.kpfu.ru/eng/?p_id=278462&p_lang=2

Resource files

File name	Size (MB)	Format
F_statya_AUTOFAGIYa_I_LC3_ASSOCIIROVANNYJ_FAGOCITOZ.pdf	2,83	pdf	show / download

Full metadata record

Field DC	Value	Language
dc.contributor.author	Ibragimov Bulat Ramilevich	ru_RU
dc.contributor.author	Skibo Yuliya Valerevna	ru_RU
dc.date.accessioned	2023-01-01T00:00:00Z	ru_RU
dc.date.available	2023-01-01T00:00:00Z	ru_RU
dc.date.issued	2023	ru_RU
dc.identifier.citation	Ибрагимов Б.Р. Аутофагия и LC3-ассоциированный фагоцитоз: сходства и различия (Обзор)/ Б.Р. Ибрагимов, Ю.В Скибо, З.И. Абрамова //Медицинская иммунология. -2023, Т. 25, № 2, стр. 233-252(Medical Immunology (Russia)/ Meditsinskaya Immunologiya) DOI: 10.15789/1563-0625-AAL-2569.	ru_RU
dc.identifier.uri	https://repository.kpfu.ru/eng/?p_id=278462&p_lang=2	ru_RU
dc.description.abstract	Медицинская иммунология	ru_RU
dc.description.abstract	Abstract. Previously, autophagy was termed as a mechanism used by the cells with a lack of essential nutrients supporting homeostasis. Over the decade of studies, autophagy proved to be a more complex, ambiguous mechanism. Its activation depends on the nature of stimulus, type of immune cells and the final result. Both canonical and non-canonical autophagy, being similar in molecular events, but showing their own distinctive features, are key processes in protecting the body from penetration of intracellular pathogens, maintaining the required level of nutrients in the cell, and removing damaged organelles and cells. Canonical autophagy probably evolved as a homeostatic response to cellular stress and nutritional deficiencies, whereas non-canonical autophagy emerged as a response to suppression of inflammation. Non-canonical autophagy, hereinafter referred to as LC3-associated phagocytosis (LAP), combines the molecular mechanism of phagocytosis with an autophagy mechanism characterized by ingestion of exogenous pathogens, formation of phagosomes (laposomes) and enhanced fusion with lysosomes, followed by degradation of their contents. Significant differences were found between the processes of LAP- and canonical autophagy, which are similar in its mechanism of action. The presence of PI3K complexes in both processes, utilization and intracellular degradation of the “cargo” which is not required for the cells and organism proceeding in the lysosomes, and involvement of almost the same proteins provide similarity of their mechanisms. However, there are differences in the initiation of the processes, e.g., different types of PI3K complexes (in autophagy, PI3K III class 1 and 2 types; in LAP PI3K III, class 3 type), usage of reactive oxygen species in LAP, different types of regulatory proteins involved (ULK1, FIP200, ATG13 , Ambra1, WIPI2, ATG14 in autophagy; and Rubicon and NOX2 in LC3-associated phagocytosis), different number of layers in the membrane structure in which lysis occurs (double-membrane autophagolysosome and single-layer membrane in laposomes) clearly depict the variety of canonical and non-canonical autophagy. The two pathways are directed for different types of biological objects, i.e., intracellular pathogens, dysfunctional proteins and organelles in autophagy, and extracellular pathogens, apoptotic bodies, bacteria, utilized in LAP, thus making these mechanisms completely different in their significance. Collectively, the new data indicate that autophagy performed via both canonical and non-canonical pathways, has evolved into a host defense mechanism capable of resisting immunological and pathogenic stress and mediating immunological tolerance to both intra- and extracellular threats. The present review discusses fundamental molecular differences between these mechanisms, as well as their role in immunity, based on the latest literature data.	ru_RU
dc.language.iso	ru	ru_RU
dc.subject	аутофагия	ru_RU
dc.subject	LC3-ассоциированный фагоцитоз	ru_RU
dc.subject	LC3	ru_RU
dc.subject	Beclin-1	ru_RU
dc.subject	Vps34	ru_RU
dc.subject	аутоиммунитет	ru_RU
dc.subject	воспаление	ru_RU
dc.title	Аутофагия и LC3-ассоциированный фагоцитоз: сходства и различия (Обзор)	ru_RU
dc.type	Articles in Russian journals and collections	ru_RU