This Research Topic is the second volume of the “Autoimmune Diabetes: Molecular Mechanisms and Neoantigens” Community Series. Please see Volume I
here.
Type 1 diabetes (T1D) is an autoimmune disease characterized by the selective and progressive destruction of the insulin-producing pancreatic beta cells by the invading immune cells. T-cells of high affinity are normally eliminated in the thymus by negative selection in order to establish central tolerance. In autoimmune diseases, impaired thymic education or low affinity T-cells are believed to be responsible for the immune attack directed against native self-proteins. Yet, there is increasing evidence that local inflammation or other forms of stress combined with genetic predisposition leads to the generation and the accumulation of aberrant or modified proteins to which central tolerance is lacking, thereby triggering autoimmunity.
This Research Topic aims at providing a comprehensive view of the dialogue between the beta cells and the immune cells during the adaptive response to inflammation and leading to the development of autoimmunity in Type 1 diabetes. A better knowledge of the different mechanisms involved in the beta cell adaptive phase will be critical to identify new therapeutic targets aiming at improving beta cell viability/function and at reducing their visibility to the immune system. The identification of new biomarkers for disease progression will be essential to define the patient immunological profile and may represent a first step toward personalized medicine.
We seek Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial, Case Report and Opinion articles that cover, but are not limited to, the following aspects of autoimmune diabetes:
• Neoantigens originating from alternative splicing, (post)-translational modification or peptide splicing/transpeptidation.
• Biomarkers of disease progression
• Beta cell stress and beta cell (dys)function/ (de)differentiation
• Cell-cell communication during inflammation and role of other pancreatic cells (endocrine and exocrine) in beta cell immunogenicity
This Research Topic is the second volume of the “Autoimmune Diabetes: Molecular Mechanisms and Neoantigens” Community Series. Please see Volume I
here.
Type 1 diabetes (T1D) is an autoimmune disease characterized by the selective and progressive destruction of the insulin-producing pancreatic beta cells by the invading immune cells. T-cells of high affinity are normally eliminated in the thymus by negative selection in order to establish central tolerance. In autoimmune diseases, impaired thymic education or low affinity T-cells are believed to be responsible for the immune attack directed against native self-proteins. Yet, there is increasing evidence that local inflammation or other forms of stress combined with genetic predisposition leads to the generation and the accumulation of aberrant or modified proteins to which central tolerance is lacking, thereby triggering autoimmunity.
This Research Topic aims at providing a comprehensive view of the dialogue between the beta cells and the immune cells during the adaptive response to inflammation and leading to the development of autoimmunity in Type 1 diabetes. A better knowledge of the different mechanisms involved in the beta cell adaptive phase will be critical to identify new therapeutic targets aiming at improving beta cell viability/function and at reducing their visibility to the immune system. The identification of new biomarkers for disease progression will be essential to define the patient immunological profile and may represent a first step toward personalized medicine.
We seek Original Research, Review, Mini-Review, Hypothesis and Theory, Perspective, Clinical Trial, Case Report and Opinion articles that cover, but are not limited to, the following aspects of autoimmune diabetes:
• Neoantigens originating from alternative splicing, (post)-translational modification or peptide splicing/transpeptidation.
• Biomarkers of disease progression
• Beta cell stress and beta cell (dys)function/ (de)differentiation
• Cell-cell communication during inflammation and role of other pancreatic cells (endocrine and exocrine) in beta cell immunogenicity