Trained innate immunity and diseases: Bane with the boon
Clinical Immunology Communications
; 2:118-129, 2022.
Article
in English
| EMBASE | ID: covidwho-2300163
ABSTRACT
Emerging research shows that innate immunity can also keep the memory of prior experiences, challenging the long-held notion that immunological memory is only the domain of the adaptive immune cells. However, the absence of immunological memory in innate immune responses has recently been brought into question. Now it is known that after a few transient activations, innate immune cells may acquire immunological memory phenotype, resulting in a stronger response to a subsequent secondary challenge. When exposed to particular microbial and/or inflammatory stimuli, trained innate immunity is characterized by the enhanced non-specific response, which is regulated by substantial metabolic alterations and epigenetic reprogramming. Trained immunity is acquired by two main reprogramming, namely, epigenetic reprogramming and metabolic adaptation/reprogramming. Epigenetic reprogramming causes changes in gene expression and cell physiology, resulting in internal cell signaling and/or accelerated and amplified cytokine release. Metabolic changes due to trained immunity induce accelerated glycolysis and glutaminolysis. As a result, trained immunity can have unfavorable outcomes, such as hyper inflammation and the development of cardiovascular diseases, autoinflammatory diseases, and neuroinflammation. In this review, the current scenario in the area of trained innate immunity, its mechanisms, and its involvement in immunological disorders are briefly outlined.Copyright © 2022
Autoimmune disorder; Epigenetic reprogramming; Inflammatory disorders; Innate immune memory; Metabolic adaptation; Trained innate immunity; adaptive immunity; Alzheimer disease/et [Etiology]; atherosclerosis/et [Etiology]; cell function; clinical outcome; coronavirus disease 2019; cytokine release; disease severity; epigenetics; gene expression; glucose metabolism; glycolysis; hematopoietic stem cell; human; immune response; immunocompetent cell; immunological memory; immunoregulation; metabolism; metastasis/et [Etiology]; multiple sclerosis/et [Etiology]; natural killer cell; nonhuman; Parkinson disease/et [Etiology]; phenotype; review; rheumatoid arthritis/et [Etiology]; sarcoidosis/et [Etiology]; signal transduction; systemic lupus erythematosus/et [Etiology]; trained immunity; tumor growth; cryopyrin/ec [Endogenous Compound]; immunosuppressive agent/an [Drug Analysis]; interleukin 12/ec [Endogenous Compound]; interleukin 15/ec [Endogenous Compound]; interleukin 18/ec [Endogenous Compound]; interleukin 1beta/ec [Endogenous Compound]; laminaran/an [Drug Analysis]; monocyte chemotactic protein 1/ec [Endogenous Compound]; sirolimus/an [Drug Analysis]; tumor necrosis factor/ec [Endogenous Compound]; unclassified drug; glutaminolysis; gsk 669/an [Drug Analysis]; gsk 717/an [Drug Analysis]; mcc 950/an [Drug Analysis]
Full text:
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Collection:
Databases of international organizations
Database:
EMBASE
Language:
English
Journal:
Clinical Immunology Communications
Year:
2022
Document Type:
Article
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