Innate immune cells (e.g., monocytes, macrophages, and mast cells) function as the first line of defense against pathogens, which are highly crucial to maintain host homeostasis. It is of great importance to fine-tune the innate immune response to pathogenic infections. Intriguingly, many regulators, including metabolic reprogramming and epigenetic modification, are responsible for governing innate immune responses.
Immune cells require a large amount of energy and metabolic intermediates to meet the requirements not only for their proliferation and survival but also for the corresponding effector functions. Besides, it is worth mentioning that pathogens can reprogram the intracellular metabolism to evade the host’s immune responses. Accumulating evidence has demonstrated that cellular metabolism orchestrates innate cell activation (e.g., macrophage); nevertheless, the cross-talk between metabolic reprogramming and innate immune responses (especially in the context of pathogenic infections) is still not comprehensively understood.
Notably, in order to survive and replicate, pathogens not only alter immune cell metabolism but also directly modify host proteins and chromatin, resulting in host epigenetic dysregulation. In turn, some innate immune signals (e.g., TLRs, RLRs, and NLRs) can also trigger dynamic chromatin alterations to regulate the expressions of activators or repressors that orchestrate pathogen elimination. Moreover, some metabolites (e.g., a-KG) can affect the epigenomes of innate immune cells (e.g., macrophages) to shape immune responses. Revealing pathogen-immune metabolism-epigenetic modification interactions is of great interest to better understand the innate immune responses to infection and seek potential therapeutic targets for infectious diseases.
In this Research Topic, we are particularly interested in the mechanisms underlying innate immune response to infection regarding metabolic reprogramming and/or epigenetic modifications.
We welcome the submission of Original Research articles, Reviews (Systematic Reviews and/or Mini-Reviews), and Perspectives strengthening our understanding of infectious diseases concerning the various aspects. The following sub-topics are chiefly encouraged:
• Metabolic reprogramming or metabolic modulation of innate immune cells in the context of pathogenic infection.
• Alterations in epigenomes of activated and quiescent innate immune cells or epigenetic modifications that modulate innate immune responses to infection.
• Cross-talk between metabolic reprogramming and epigenetic modifications in innate immune response to infection.
• Exploration and validation of novel and promising therapeutic targets for pathogenic infection-related diseases.
Innate immune cells (e.g., monocytes, macrophages, and mast cells) function as the first line of defense against pathogens, which are highly crucial to maintain host homeostasis. It is of great importance to fine-tune the innate immune response to pathogenic infections. Intriguingly, many regulators, including metabolic reprogramming and epigenetic modification, are responsible for governing innate immune responses.
Immune cells require a large amount of energy and metabolic intermediates to meet the requirements not only for their proliferation and survival but also for the corresponding effector functions. Besides, it is worth mentioning that pathogens can reprogram the intracellular metabolism to evade the host’s immune responses. Accumulating evidence has demonstrated that cellular metabolism orchestrates innate cell activation (e.g., macrophage); nevertheless, the cross-talk between metabolic reprogramming and innate immune responses (especially in the context of pathogenic infections) is still not comprehensively understood.
Notably, in order to survive and replicate, pathogens not only alter immune cell metabolism but also directly modify host proteins and chromatin, resulting in host epigenetic dysregulation. In turn, some innate immune signals (e.g., TLRs, RLRs, and NLRs) can also trigger dynamic chromatin alterations to regulate the expressions of activators or repressors that orchestrate pathogen elimination. Moreover, some metabolites (e.g., a-KG) can affect the epigenomes of innate immune cells (e.g., macrophages) to shape immune responses. Revealing pathogen-immune metabolism-epigenetic modification interactions is of great interest to better understand the innate immune responses to infection and seek potential therapeutic targets for infectious diseases.
In this Research Topic, we are particularly interested in the mechanisms underlying innate immune response to infection regarding metabolic reprogramming and/or epigenetic modifications.
We welcome the submission of Original Research articles, Reviews (Systematic Reviews and/or Mini-Reviews), and Perspectives strengthening our understanding of infectious diseases concerning the various aspects. The following sub-topics are chiefly encouraged:
• Metabolic reprogramming or metabolic modulation of innate immune cells in the context of pathogenic infection.
• Alterations in epigenomes of activated and quiescent innate immune cells or epigenetic modifications that modulate innate immune responses to infection.
• Cross-talk between metabolic reprogramming and epigenetic modifications in innate immune response to infection.
• Exploration and validation of novel and promising therapeutic targets for pathogenic infection-related diseases.
