Immune homeostasis results from a balance between effector and regulatory T (Treg) cells. In particular, Th17 cells and Treg cells have opposing functions and are key to maintaining immune homeostasis. In autoimmune diseases, their stability, plasticity and function are dysregulated and the balance between both subsets is disturbed. Recent studies have demonstrated that an imbalance between pathogenic Th17 and Treg cells contributes to the development of various autoimmune diseases, including multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), as well as rheumatoid arthritis (RA) and collagen type II-induced arthritis (CIA). However, the molecular mechanisms responsible for Th17 and Treg cell dysregulation remain largely unknown. Metabolic and environmental factors seem to play a role in the imbalance between Th17 cells and Treg cells. For example, high salt consumption can promote the development of pathogenic autoimmune Th17 cells, inhibit the suppressive function of Treg cells and aggravate autoimmune diseases. Moreover, vitamin D deficiency has also been linked to autoimmunity. Revealing the underlying mechanisms will help to identify new targets for the treatment of autoimmune diseases.
Present the problem that you would like to tackle in this Research topic and what can be done to achieve it including recent advances.
The aim of this Research Topic is to improve our understanding of Th17 and Treg cell dysregulation in autoimmunity. A better knowledge of Treg cell subsets and of their plasticity, is required to decipher their contribution to uncontrolled autoimmune responses. Moreover, Th17 cells can develop a pathogenic or immune tolerant phenotype. The plasticity and function of these T cell subsets are regulated by a variety of environmental and metabolic factors. Articles that are part of this collection will provide new insights into these regulatory mechanisms.
We welcome the submission of Original Research, Review and Mini-review articles that improve our understanding of Th17 and Treg cell dysregulation in autoimmune diseases. Topic areas of interest include, but are not limited to:
1. Molecular mechanisms that regulate the function, stability and plasticity of Treg cells and Th17 cells in health and autoimmune diseases
2. Environmental factors that modulate the balance between Treg cells and Th17 cells
3. New surface markers and transcription factors that help identifying different subpopulations of Treg cells in autoimmune diseases
4. Changes in the JAK/STAT signaling pathways and their implication in Th17 cell differentiation
5. Expansion of Treg cell populations as an experimental therapeutic approach to control autoimmune diseases
6. Molecular mechanisms regulating Treg cell and effector T cell migration into inflamed tissues
Immune homeostasis results from a balance between effector and regulatory T (Treg) cells. In particular, Th17 cells and Treg cells have opposing functions and are key to maintaining immune homeostasis. In autoimmune diseases, their stability, plasticity and function are dysregulated and the balance between both subsets is disturbed. Recent studies have demonstrated that an imbalance between pathogenic Th17 and Treg cells contributes to the development of various autoimmune diseases, including multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), as well as rheumatoid arthritis (RA) and collagen type II-induced arthritis (CIA). However, the molecular mechanisms responsible for Th17 and Treg cell dysregulation remain largely unknown. Metabolic and environmental factors seem to play a role in the imbalance between Th17 cells and Treg cells. For example, high salt consumption can promote the development of pathogenic autoimmune Th17 cells, inhibit the suppressive function of Treg cells and aggravate autoimmune diseases. Moreover, vitamin D deficiency has also been linked to autoimmunity. Revealing the underlying mechanisms will help to identify new targets for the treatment of autoimmune diseases.
Present the problem that you would like to tackle in this Research topic and what can be done to achieve it including recent advances.
The aim of this Research Topic is to improve our understanding of Th17 and Treg cell dysregulation in autoimmunity. A better knowledge of Treg cell subsets and of their plasticity, is required to decipher their contribution to uncontrolled autoimmune responses. Moreover, Th17 cells can develop a pathogenic or immune tolerant phenotype. The plasticity and function of these T cell subsets are regulated by a variety of environmental and metabolic factors. Articles that are part of this collection will provide new insights into these regulatory mechanisms.
We welcome the submission of Original Research, Review and Mini-review articles that improve our understanding of Th17 and Treg cell dysregulation in autoimmune diseases. Topic areas of interest include, but are not limited to:
1. Molecular mechanisms that regulate the function, stability and plasticity of Treg cells and Th17 cells in health and autoimmune diseases
2. Environmental factors that modulate the balance between Treg cells and Th17 cells
3. New surface markers and transcription factors that help identifying different subpopulations of Treg cells in autoimmune diseases
4. Changes in the JAK/STAT signaling pathways and their implication in Th17 cell differentiation
5. Expansion of Treg cell populations as an experimental therapeutic approach to control autoimmune diseases
6. Molecular mechanisms regulating Treg cell and effector T cell migration into inflamed tissues
