Chronic inflammation and aging are intricately linked processes that significantly impact human health. During the aging process, the immune system undergoes a series of alterations collectively known as immunosenescence, leading to impaired immune responses and increased susceptibility to infections and chronic inflammatory diseases. T cells, as vital components in maintaining immune homeostasis, play a crucial role in pathogen recognition, eradication, and immune surveillance against cancer cells. In conditions marked by chronic inflammation, such as rheumatoid arthritis, inflammatory bowel disease, and atherosclerosis, T cells often exhibit persistent activation. This sustained activation contributes to tissue damage and exacerbates inflammatory responses, ultimately driving disease progression. Likewise, in aging individuals, T cells manifest characteristic alterations including decreased production of naïve T cells, accumulation of memory T cells, and a narrowed T cell receptor repertoire. These changes culminate in diminished immune function, compromised pathogen clearance, and heightened susceptibility to infections and malignancies. Factors such as chronic antigenic stimulation, microenvironmental alterations, dysregulated signaling pathways, and changes in epigenetic regulation collectively contribute to T cell dysfunction. Investigating the mechanisms underlying T cell immunity in chronic inflammation and aging represents a critical area of research with significant clinical implications.
In conclusion, the dysfunction of T cells in the context of chronic inflammation and age-related diseases is a complex phenomenon with significant clinical implications. It is crucial to obtain a comprehensive understanding of the underlying mechanisms driving T cell dysfunction to develop effective therapeutic strategies. Therefore, the objective of this research theme is to delve deep into the cellular and molecular cues that contribute to the impairment of T cell function in different disease conditions associated with chronic inflammation and aging. By unraveling the intricacies of T cell dysfunction, this research aims to shed light on the specific mechanisms that disrupt T cell homeostasis and compromise their ability to mount effective immune responses. Understanding the cellular factors, signaling pathways, and regulatory mechanisms that drive T cell dysfunction will provide valuable insights into disease pathogenesis.
This Research Topic accepts Original Research, Systematic Review, Methods, Review and Mini-Review, Perspective, Brief Research Report, and Opinion. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
• Impact of chronic inflammation on T cell activation, differentiation, and function.
• Role of T cell exhaustion and senescence in chronic inflammatory diseases and aging.
• Mechanisms underlying impaired T cell responses in chronic inflammation and aging.
• Dysregulation of immune checkpoints in T cell dysfunction during chronic inflammation and aging.
• Influence of the aging microenvironment on T cell function and immune responses.
• Epigenetic and metabolic basis of T cell dysfunction in chronic inflammation and aging.
• Potential therapeutic strategies to restore T cell function and immune homeostasis in chronic inflammation and aging.
• Building better animal models to unravel mechanisms underlying T cell defects in chronic inflammation and aging.
All Topic Editors declare no competing interests with regard to the Research Topic subject
Keywords:
T cell, maintenance, homeostasis, Chronic inflammation, Immunosenescence, Inflammaging, T cell activation, T cell differentiation, Effector T cells, regulatory T cells, Immune-mediated pathologies, T cell exhaustion, T cell terminal differentiation, T cel
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Chronic inflammation and aging are intricately linked processes that significantly impact human health. During the aging process, the immune system undergoes a series of alterations collectively known as immunosenescence, leading to impaired immune responses and increased susceptibility to infections and chronic inflammatory diseases. T cells, as vital components in maintaining immune homeostasis, play a crucial role in pathogen recognition, eradication, and immune surveillance against cancer cells. In conditions marked by chronic inflammation, such as rheumatoid arthritis, inflammatory bowel disease, and atherosclerosis, T cells often exhibit persistent activation. This sustained activation contributes to tissue damage and exacerbates inflammatory responses, ultimately driving disease progression. Likewise, in aging individuals, T cells manifest characteristic alterations including decreased production of naïve T cells, accumulation of memory T cells, and a narrowed T cell receptor repertoire. These changes culminate in diminished immune function, compromised pathogen clearance, and heightened susceptibility to infections and malignancies. Factors such as chronic antigenic stimulation, microenvironmental alterations, dysregulated signaling pathways, and changes in epigenetic regulation collectively contribute to T cell dysfunction. Investigating the mechanisms underlying T cell immunity in chronic inflammation and aging represents a critical area of research with significant clinical implications.
In conclusion, the dysfunction of T cells in the context of chronic inflammation and age-related diseases is a complex phenomenon with significant clinical implications. It is crucial to obtain a comprehensive understanding of the underlying mechanisms driving T cell dysfunction to develop effective therapeutic strategies. Therefore, the objective of this research theme is to delve deep into the cellular and molecular cues that contribute to the impairment of T cell function in different disease conditions associated with chronic inflammation and aging. By unraveling the intricacies of T cell dysfunction, this research aims to shed light on the specific mechanisms that disrupt T cell homeostasis and compromise their ability to mount effective immune responses. Understanding the cellular factors, signaling pathways, and regulatory mechanisms that drive T cell dysfunction will provide valuable insights into disease pathogenesis.
This Research Topic accepts Original Research, Systematic Review, Methods, Review and Mini-Review, Perspective, Brief Research Report, and Opinion. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
• Impact of chronic inflammation on T cell activation, differentiation, and function.
• Role of T cell exhaustion and senescence in chronic inflammatory diseases and aging.
• Mechanisms underlying impaired T cell responses in chronic inflammation and aging.
• Dysregulation of immune checkpoints in T cell dysfunction during chronic inflammation and aging.
• Influence of the aging microenvironment on T cell function and immune responses.
• Epigenetic and metabolic basis of T cell dysfunction in chronic inflammation and aging.
• Potential therapeutic strategies to restore T cell function and immune homeostasis in chronic inflammation and aging.
• Building better animal models to unravel mechanisms underlying T cell defects in chronic inflammation and aging.
All Topic Editors declare no competing interests with regard to the Research Topic subject
Keywords:
T cell, maintenance, homeostasis, Chronic inflammation, Immunosenescence, Inflammaging, T cell activation, T cell differentiation, Effector T cells, regulatory T cells, Immune-mediated pathologies, T cell exhaustion, T cell terminal differentiation, T cel
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.