The immune system protects against invading pathogens, ageing and cancer. Engagement of immune cells by antigens prompts cellular responses: activation, proliferation, and differentiation. These responses are regulated through an elaborate combination of genetic, epigenetic, molecular, and cellular mechanisms. Such mechanisms vary depending on cell types, states of development and activation, and type, stage or tempo of the immune response. At any level, failure of a regulatory mechanism(s) can lead to disease. For example, diseases can be caused by inadequate or violent immune responses or by aberrant responses to self. Many, though not all, factors that underpin or exacerbate regulatory defects are known. However, the precise cause of such defects and how they, in turn, cause specific pathological processes remain debated and are under scientific investigation. This edition will explore known defects, causes, and how they correspond to specific pathological processes in chronic inflammatory diseases. The issue will also explore potential therapeutic strategies.
An efficient immune system is pivotal for health. The system, however, can fail to provide effective immunity or may contribute to chronic inflammatory diseases by failing to be restrained by regulatory mechanisms. In recent years, a wealth of information has accumulated on potential lesions in the evolution and regulation of the immune system. However, there is little in the way of agreement as to how such defects promote immune mediated pathology and, in particular, which specific mechanisms underpin chronic inflammatory diseases. The main aim of the proposed edition of this journal will be to provide an overview of evidence on the genetic, molecular and cellular bases of defective immune regulation in relation to specific pathologic processes in chronic inflammatory diseases. For example, a great many autoimmune diseases manifest in the production of autoantibodies, excessive production of pro-inflammatory cytokines and defective regulatory immune cells and pathways yet the direct immunopathology differs from disease to disease. This issue is intended to explore how the pathways that underpin defective regulation of the immune system promote specific pathological events in patients and how such knowledge can be employed to define new therapeutic strategies.
This Research Topic welcomes Review and Original Research articles related to mechanisms of immune regulation, how these fail at genetic, molecular and cellular levels and how such specific defects lead to specific disease mechanisms in chronic inflammatory diseases. Themes could include, but are not limited to:
• genetic/epigenetic regulation
• intracellular signaling
• metabolic programming
• mechanisms of cellular interactions involved in defective immune regulation, immunological tolerance , and effector immunity
• specific defects in immune regulation associated with specific pathogenic mechanisms.
• how known defects in immune regulation promote and/or contribute directly to pathogenic mechanisms associated with chronic inflammatory diseases
The immune system protects against invading pathogens, ageing and cancer. Engagement of immune cells by antigens prompts cellular responses: activation, proliferation, and differentiation. These responses are regulated through an elaborate combination of genetic, epigenetic, molecular, and cellular mechanisms. Such mechanisms vary depending on cell types, states of development and activation, and type, stage or tempo of the immune response. At any level, failure of a regulatory mechanism(s) can lead to disease. For example, diseases can be caused by inadequate or violent immune responses or by aberrant responses to self. Many, though not all, factors that underpin or exacerbate regulatory defects are known. However, the precise cause of such defects and how they, in turn, cause specific pathological processes remain debated and are under scientific investigation. This edition will explore known defects, causes, and how they correspond to specific pathological processes in chronic inflammatory diseases. The issue will also explore potential therapeutic strategies.
An efficient immune system is pivotal for health. The system, however, can fail to provide effective immunity or may contribute to chronic inflammatory diseases by failing to be restrained by regulatory mechanisms. In recent years, a wealth of information has accumulated on potential lesions in the evolution and regulation of the immune system. However, there is little in the way of agreement as to how such defects promote immune mediated pathology and, in particular, which specific mechanisms underpin chronic inflammatory diseases. The main aim of the proposed edition of this journal will be to provide an overview of evidence on the genetic, molecular and cellular bases of defective immune regulation in relation to specific pathologic processes in chronic inflammatory diseases. For example, a great many autoimmune diseases manifest in the production of autoantibodies, excessive production of pro-inflammatory cytokines and defective regulatory immune cells and pathways yet the direct immunopathology differs from disease to disease. This issue is intended to explore how the pathways that underpin defective regulation of the immune system promote specific pathological events in patients and how such knowledge can be employed to define new therapeutic strategies.
This Research Topic welcomes Review and Original Research articles related to mechanisms of immune regulation, how these fail at genetic, molecular and cellular levels and how such specific defects lead to specific disease mechanisms in chronic inflammatory diseases. Themes could include, but are not limited to:
• genetic/epigenetic regulation
• intracellular signaling
• metabolic programming
• mechanisms of cellular interactions involved in defective immune regulation, immunological tolerance , and effector immunity
• specific defects in immune regulation associated with specific pathogenic mechanisms.
• how known defects in immune regulation promote and/or contribute directly to pathogenic mechanisms associated with chronic inflammatory diseases