T cells are the gatekeepers of infection control and tumor development, and are critical for maintaining immune homeostasis. Inflammatory cytokines are necessary for optimal T cell activation and differentiation. However, prolonged inflammation can drive T cell dysfunction. Recent studies have revealed that continuous exposure to antigens and inflammatory signals leads to CD8+ T cell exhaustion: a state of non-responsiveness that curtails their cytotoxic effector functions. Likewise, CD4+ T cells are debilitated by persistent inflammatory cues. Furthermore, chronically stimulated T regulatory cells (Tregs) have destabilized Foxp3 expression, leading to irreversible functional defect and a breakdown of immune tolerance. As a result, T cell dysfunction driven by sustained inflammation forms the common pathological basis for many chronic inflammatory conditions, including autoimmune diseases, cancer and chronic viral infections. Hence, an in-depth comprehension of how chronic inflammatory processes influence T cell differentiation and function will provide the foundation for future therapies that restore T cell responses and immune homeostasis in multiple chronic diseases.
This Research Topic is focused on the mechanisms of T cell dysfunction driven by the cytokine and metabolic milieu in different chronic inflammatory diseases, with the goal of harnessing such knowledge to advance therapeutic interventions. We welcome the submission of Original Research, Review, Mini-Review, Perspective, Clinical Trial, and Case Report articles that cover, but are not limited to, the following topics:
- Molecular mechanisms of T cell exhaustion in various chronic inflammatory diseases
- Molecular mechanisms of Treg dysfunction in various chronic inflammatory diseases
- The impact of chronic inflammation on T cell metabolism
- Factors that perpetuate chronic inflammation in different pathological conditions
- Therapeutic interventions to enhance T cell function in chronic inflammatory diseases
T cells are the gatekeepers of infection control and tumor development, and are critical for maintaining immune homeostasis. Inflammatory cytokines are necessary for optimal T cell activation and differentiation. However, prolonged inflammation can drive T cell dysfunction. Recent studies have revealed that continuous exposure to antigens and inflammatory signals leads to CD8+ T cell exhaustion: a state of non-responsiveness that curtails their cytotoxic effector functions. Likewise, CD4+ T cells are debilitated by persistent inflammatory cues. Furthermore, chronically stimulated T regulatory cells (Tregs) have destabilized Foxp3 expression, leading to irreversible functional defect and a breakdown of immune tolerance. As a result, T cell dysfunction driven by sustained inflammation forms the common pathological basis for many chronic inflammatory conditions, including autoimmune diseases, cancer and chronic viral infections. Hence, an in-depth comprehension of how chronic inflammatory processes influence T cell differentiation and function will provide the foundation for future therapies that restore T cell responses and immune homeostasis in multiple chronic diseases.
This Research Topic is focused on the mechanisms of T cell dysfunction driven by the cytokine and metabolic milieu in different chronic inflammatory diseases, with the goal of harnessing such knowledge to advance therapeutic interventions. We welcome the submission of Original Research, Review, Mini-Review, Perspective, Clinical Trial, and Case Report articles that cover, but are not limited to, the following topics:
- Molecular mechanisms of T cell exhaustion in various chronic inflammatory diseases
- Molecular mechanisms of Treg dysfunction in various chronic inflammatory diseases
- The impact of chronic inflammation on T cell metabolism
- Factors that perpetuate chronic inflammation in different pathological conditions
- Therapeutic interventions to enhance T cell function in chronic inflammatory diseases