Recent advances in inflammation biology have revealed that immune responses are highly dynamic and context-dependent, shaped by the nature of the inflammatory stimulus, the tissue microenvironment, host metabolic status, microbial interactions, and disease stage. Rather than a uniform cascade, inflammation is now recognized as a spatially and temporally tailored process, with distinct molecular and cellular programs governing its initiation, propagation, resolution or chronicity. This nuanced view of inflammation is transforming our understanding of immune regulation in both health and disease.
However, a central challenge persists: why does inflammation resolve effectively in some contexts while progressing to chronic pathology in others? For instance, tissue-specific immune cells exhibit diverse transcriptional and metabolic profiles that influence their inflammatory responses. Non-immune cells such as epithelial, stromal, and endothelial cells also contribute actively to shaping these local immune environments. Moreover, extrinsic factors, such as circadian rhythms, dietary signals, and microbiota-derived metabolites, modulate inflammatory tone and resolution capacity in a context-dependent manner.
The failure to resolve inflammation is a driving force behind many chronic diseases, including autoimmunity, fibrosis, cardiovascular disease, neuroinflammation, and cancer. Despite major therapeutic advances, many interventions still target generalized inflammatory mechanisms rather than addressing the specific context in which inflammation occurs. There is a critical need to deepen our mechanistic understanding of how inflammation is modulated across different tissues and physiological states, and how this knowledge can be harnessed to design context-aware immunotherapies.
The primary aim of this Research Topic is to illuminate how inflammatory responses are governed by local and systemic context; across tissues, time scales, and disease conditions. By bringing together research that deciphers mechanisms of immune adaptation, cellular plasticity, and tissue-specific signaling during inflammation, we aim to uncover unifying principles and clinically relevant differences in inflammatory programming. Ultimately, this collection seeks to guide development of more precise, tissue- and disease-tailored anti-inflammatory strategies that preserve immune function while promoting resolution and repair.
Topics of Interest Include, but are not limited to:
• Tissue-specific regulation of inflammation and resolution
• Plasticity and metabolic reprogramming of innate and adaptive immune cells in different microenvironments
• Role of stromal, epithelial, and endothelial cells in modulating immune responses
• Crosstalk between inflammation, regeneration, and fibrosis in distinct organs
• Influence of circadian rhythms, diet, and the microbiota on inflammatory trajectories
• Mechanisms underlying successful vs. failed resolution of inflammation
• Comparative studies of sterile vs. infectious inflammation
• Immunological imprinting and memory of inflammatory events
• Biomarkers for context-specific inflammation and resolution status
• Targeting inflammatory circuits with tissue-adapted or disease-specific immunomodulators
Recent advances in inflammation biology have revealed that immune responses are highly dynamic and context-dependent, shaped by the nature of the inflammatory stimulus, the tissue microenvironment, host metabolic status, microbial interactions, and disease stage. Rather than a uniform cascade, inflammation is now recognized as a spatially and temporally tailored process, with distinct molecular and cellular programs governing its initiation, propagation, resolution or chronicity. This nuanced view of inflammation is transforming our understanding of immune regulation in both health and disease.
However, a central challenge persists: why does inflammation resolve effectively in some contexts while progressing to chronic pathology in others? For instance, tissue-specific immune cells exhibit diverse transcriptional and metabolic profiles that influence their inflammatory responses. Non-immune cells such as epithelial, stromal, and endothelial cells also contribute actively to shaping these local immune environments. Moreover, extrinsic factors, such as circadian rhythms, dietary signals, and microbiota-derived metabolites, modulate inflammatory tone and resolution capacity in a context-dependent manner.
The failure to resolve inflammation is a driving force behind many chronic diseases, including autoimmunity, fibrosis, cardiovascular disease, neuroinflammation, and cancer. Despite major therapeutic advances, many interventions still target generalized inflammatory mechanisms rather than addressing the specific context in which inflammation occurs. There is a critical need to deepen our mechanistic understanding of how inflammation is modulated across different tissues and physiological states, and how this knowledge can be harnessed to design context-aware immunotherapies.
The primary aim of this Research Topic is to illuminate how inflammatory responses are governed by local and systemic context; across tissues, time scales, and disease conditions. By bringing together research that deciphers mechanisms of immune adaptation, cellular plasticity, and tissue-specific signaling during inflammation, we aim to uncover unifying principles and clinically relevant differences in inflammatory programming. Ultimately, this collection seeks to guide development of more precise, tissue- and disease-tailored anti-inflammatory strategies that preserve immune function while promoting resolution and repair.
Topics of Interest Include, but are not limited to:
• Tissue-specific regulation of inflammation and resolution
• Plasticity and metabolic reprogramming of innate and adaptive immune cells in different microenvironments
• Role of stromal, epithelial, and endothelial cells in modulating immune responses
• Crosstalk between inflammation, regeneration, and fibrosis in distinct organs
• Influence of circadian rhythms, diet, and the microbiota on inflammatory trajectories
• Mechanisms underlying successful vs. failed resolution of inflammation
• Comparative studies of sterile vs. infectious inflammation
• Immunological imprinting and memory of inflammatory events
• Biomarkers for context-specific inflammation and resolution status
• Targeting inflammatory circuits with tissue-adapted or disease-specific immunomodulators