Autoimmunity in older adults is a burgeoning field of research that seeks to understand the complex interplay between aging and the immune system. As individuals age, there is a notable decline in the naïve T cell pool, a constriction of the T cell receptor (TCR) repertoire, and a clonal expansion of memory T cells. These immunological changes contribute to age-related immunodeficiency and dysfunction, particularly in genetically susceptible individuals exposed to various environmental factors. This can lead to an increased expansion of homeostatic T cells against autoantigens. Additionally, the decline in sex hormone levels, loss of tissue homeostasis, and a heightened state of inflammation with age can further modulate adaptive immune responses. These processes are implicated in the development of autoimmune diseases such as rheumatoid arthritis, primary Sjögren's syndrome, multiple sclerosis, myasthenia gravis, and giant cell arteritis, typically manifesting in the fifth decade of life. Despite ongoing research, there remains a significant gap in understanding the precise molecular mechanisms driving these changes, necessitating further investigation.
This research topic aims to explore the current research identifying the role of environmental and host factors, such as sex hormones, in modulating immune responses in older adults with autoimmune diseases. A particular focus is on the increase of age-associated T and B cells and their contribution to autoimmunity. Understanding the molecular mechanisms behind the proliferation of these adaptive immune cells is crucial for elucidating the pathogenesis of autoimmunity. This knowledge is essential for developing novel small-molecule inhibitors or repurposing existing drugs. Additionally, the adaptation of newer omics methods at the single-cell level is anticipated to significantly enhance research in this area.
To gather further insights into the mechanisms and interventions for autoimmunity in older adults, we welcome articles addressing, but not limited to, the following themes:
- Role of B-cells in the development of autoimmunity
- Epigenetic changes of immune cells driven by sex hormones
- Single-cell genomics in identifying homeostatic expansion of age-related T-cells
- Genetic predisposition causing overaction of adaptive immune response in elderly autoimmune women
- Telomerase deficiency in autoimmunity
- Immunomodulatory effects of aging interventions in autoimmune conditions
- Therapeutic strategies for autoimmunity in aging adults
- Inflammatory cells and pathways in aging and autoimmunity.
Keywords:
Immunosenescence, Autoimmune Disease, Sex Hormones, Epigenetics, Single Cell Genomics
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.
Autoimmunity in older adults is a burgeoning field of research that seeks to understand the complex interplay between aging and the immune system. As individuals age, there is a notable decline in the naïve T cell pool, a constriction of the T cell receptor (TCR) repertoire, and a clonal expansion of memory T cells. These immunological changes contribute to age-related immunodeficiency and dysfunction, particularly in genetically susceptible individuals exposed to various environmental factors. This can lead to an increased expansion of homeostatic T cells against autoantigens. Additionally, the decline in sex hormone levels, loss of tissue homeostasis, and a heightened state of inflammation with age can further modulate adaptive immune responses. These processes are implicated in the development of autoimmune diseases such as rheumatoid arthritis, primary Sjögren's syndrome, multiple sclerosis, myasthenia gravis, and giant cell arteritis, typically manifesting in the fifth decade of life. Despite ongoing research, there remains a significant gap in understanding the precise molecular mechanisms driving these changes, necessitating further investigation.
This research topic aims to explore the current research identifying the role of environmental and host factors, such as sex hormones, in modulating immune responses in older adults with autoimmune diseases. A particular focus is on the increase of age-associated T and B cells and their contribution to autoimmunity. Understanding the molecular mechanisms behind the proliferation of these adaptive immune cells is crucial for elucidating the pathogenesis of autoimmunity. This knowledge is essential for developing novel small-molecule inhibitors or repurposing existing drugs. Additionally, the adaptation of newer omics methods at the single-cell level is anticipated to significantly enhance research in this area.
To gather further insights into the mechanisms and interventions for autoimmunity in older adults, we welcome articles addressing, but not limited to, the following themes:
- Role of B-cells in the development of autoimmunity
- Epigenetic changes of immune cells driven by sex hormones
- Single-cell genomics in identifying homeostatic expansion of age-related T-cells
- Genetic predisposition causing overaction of adaptive immune response in elderly autoimmune women
- Telomerase deficiency in autoimmunity
- Immunomodulatory effects of aging interventions in autoimmune conditions
- Therapeutic strategies for autoimmunity in aging adults
- Inflammatory cells and pathways in aging and autoimmunity.
Keywords:
Immunosenescence, Autoimmune Disease, Sex Hormones, Epigenetics, Single Cell Genomics
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.