About this Research Topic
This Research Topic is the second volume of the “Regulators of Immune System Function in Autoimmunity and Aging - Molecular and Cellular Research” Community Series. Please see Volume I here
Fundamental biological processes of autoimmunity and aging, including dysregulated immune susceptible factors and environmental factors underlie the risk for the onset of multiple age-related diseases as well as tissue and organ damage. The etiology of both these processes remains incompletely understood, although it is well-accepted that they are attributed to a combination of genetic and environmental factors. More recently, a role for inherited epigenetic changes has also been demonstrated. Epigenetic mechanisms may serve as a dynamic link between the environment, genotype, and phenotype. Side effects may vary between individuals due to innate differences in genetic/epigenetic makeup. For this reason, it is very important to find which inter-individual genetic as well as epigenetic variants regulate individual immunological factors. The interaction between genetic/epigenetic modifications and key immunological factors is a critical area of research and may provide potential therapeutic targets for autoimmune and age-related diseases.
Genome-wide association studies (GWAS) have identified multiple autoimmune and age-related disease risk loci but they represent only an early step in the understanding of its pathogenesis. Functional polymorphisms in immune-related genes (such as HLA, cytokines and their receptors, TLRs, BCR, CD40, signaling effectors, and those involved in central tolerance) may lead to the activation of dendritic cells (DCs) and autoreactive T cells, defects in Treg cell development and dysregulated B cell signaling. This can lead to tissue injury and clinical disease. In age-related autoimmune pathologies, senescent cells secrete inflammation-associated factors such as IL-1, IL-6, IL-8, IL-17, and TNF-α, referred to as immune-risk phenotype (IRP) or senescence-associated secretory phenotypes (SASP). This phenotype is likely dictated, not only by ‘incorrect’ cytokine production but also defects in activation-induced cell death and T cell subset imbalances. Autoimmunity and aging susceptibility, genes, and the environment are all involved in the generation of aberrant epigenetic profiles in a cell-specific manner, which ultimately results in dysregulation of gene expression. These changes in the epigenetic profile of cells influence the activity of the immune system. Although the exact immune-pathological mechanism of autoimmune and age-related diseases is not fully understood, numerous investigations have demonstrated abnormalities in both the innate and the adaptive systems, which are important in driving the inflammatory process. Understanding the structure and dynamics of molecular networks is extremely important for a better understanding of these processes as further analysis will not only provide support in research on autoimmune and age-related diseases but also optimize their treatment.
We welcome authors to submit Original Research, Systematic Review, Review, Mini Review, and Perspective articles focusing on, but not limited to:
• Molecular analysis and functional studies in different diseases and age groups, as well as in different tissue types, which will supply the details necessary to comprehend these processes
• Research focused on getting to know the nature of the defect of autoimmune and age-related diseases and the correlation between the clinical picture and the genotype of the disease
• Discovery of new subset of T and B cells in age-related diseases and autoimmunity
• Personalized medicine – enhancing the knowledge on safe and effective therapy based on genetic backgrounds and epigenetic impacts and consequently development of new therapeutic strategies for patients with drug resistance/other side effects.
The Topic Editors declare no competing interests with regard to the Research Topic subject.
Fundamental biological processes of autoimmunity and aging, including dysregulated immune susceptible factors and environmental factors underlie the risk for the onset of multiple age-related diseases as well as tissue and organ damage. The etiology of both these processes remains incompletely understood, although it is well-accepted that they are attributed to a combination of genetic and environmental factors. More recently, a role for inherited epigenetic changes has also been demonstrated. Epigenetic mechanisms may serve as a dynamic link between the environment, genotype, and phenotype. Side effects may vary between individuals due to innate differences in genetic/epigenetic makeup. For this reason, it is very important to find which inter-individual genetic as well as epigenetic variants regulate individual immunological factors. The interaction between genetic/epigenetic modifications and key immunological factors is a critical area of research and may provide potential therapeutic targets for autoimmune and age-related diseases.
Genome-wide association studies (GWAS) have identified multiple autoimmune and age-related disease risk loci but they represent only an early step in the understanding of its pathogenesis. Functional polymorphisms in immune-related genes (such as HLA, cytokines and their receptors, TLRs, BCR, CD40, signaling effectors, and those involved in central tolerance) may lead to the activation of dendritic cells (DCs) and autoreactive T cells, defects in Treg cell development and dysregulated B cell signaling. This can lead to tissue injury and clinical disease. In age-related autoimmune pathologies, senescent cells secrete inflammation-associated factors such as IL-1, IL-6, IL-8, IL-17, and TNF-α, referred to as immune-risk phenotype (IRP) or senescence-associated secretory phenotypes (SASP). This phenotype is likely dictated, not only by ‘incorrect’ cytokine production but also defects in activation-induced cell death and T cell subset imbalances. Autoimmunity and aging susceptibility, genes, and the environment are all involved in the generation of aberrant epigenetic profiles in a cell-specific manner, which ultimately results in dysregulation of gene expression. These changes in the epigenetic profile of cells influence the activity of the immune system. Although the exact immune-pathological mechanism of autoimmune and age-related diseases is not fully understood, numerous investigations have demonstrated abnormalities in both the innate and the adaptive systems, which are important in driving the inflammatory process. Understanding the structure and dynamics of molecular networks is extremely important for a better understanding of these processes as further analysis will not only provide support in research on autoimmune and age-related diseases but also optimize their treatment.
We welcome authors to submit Original Research, Systematic Review, Review, Mini Review, and Perspective articles focusing on, but not limited to:
• Molecular analysis and functional studies in different diseases and age groups, as well as in different tissue types, which will supply the details necessary to comprehend these processes
• Research focused on getting to know the nature of the defect of autoimmune and age-related diseases and the correlation between the clinical picture and the genotype of the disease
• Discovery of new subset of T and B cells in age-related diseases and autoimmunity
• Personalized medicine – enhancing the knowledge on safe and effective therapy based on genetic backgrounds and epigenetic impacts and consequently development of new therapeutic strategies for patients with drug resistance/other side effects.
The Topic Editors declare no competing interests with regard to the Research Topic subject.
Keywords: autoimmunity, aging, immune factors, signaling pathways, genetics, epigenetics
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.
