Type 1 diabetes is a general term that describes a condition - usually found in children - which causes immune-mediated pancreatic beta-cell destruction and lifetime insulin use. Claims of a cure around the corner have been made over the past 30 years with little advancement to show for the hundreds of millions of research dollars spent on both basic science experimentation and clinical research trials. In this regard, it is true to say science and medicine slowly evolves and knowledge gaps get filled incrementally over time. Real breakthrough can happen in a moment but is often the culmination of pain staking detailed work, accident, and inspiration.
The 21st century offers science and medicine a cadre of new tools and insights that is enabling us to tackle problems like type 1 diabetes in a highly personalized way with a depth of knowledge previously unachievable. Such areas of knowledge development include the use of gene editing techniques, access to genomic, proteomic, metabolomic, and epigenetic screens that produce large, detailed datasets, and bioinformatic tools that allow these massive datasets to be interrogated and annotated into meaningful information. These new tools are rapidly changing our ability to understand disease states and recognize that our phenotypic description of a disease like type 1 diabetes is a generalization of complex molecular diseases that harbor both meaningful differences and common immunological themes among patients.
The present issue of Frontiers in Immunology will take a bold step towards uncovering our knowledge gaps in the field of type 1 diabetes and describe new approaches to tackling one of our most challenging aspects of human molecular biology, that being an in-depth understanding of alterations in immune function that leads to immune-mediated diabetes.
As we begin to use our new toolbox to fill gaps in knowledge, we can answer questions such as; how pancreatic beta-cell death occurs, what effector cell populations are responsible for beta-cell death, what are the defects in type 1 diabetes regulatory cell populations that allow for a hostile environment, how does the host microbiome interact with the immune system to create a hostile immune environment, and what genetic or epigenetic elements can be manipulated to forestall or prevent disease in susceptible individuals. Equally important, we can learn about new biomarkers and therapeutic targets that might benefit identification of pre-diabetic children who can ultimately have their immune systems re-routed away from their inherent disease trajectory.
This Research Topic welcomes articles focusing on, but not limited to, the following aspects of immune-mediated diabetes:
• Effector cell populations gone awry; how do effector cells kill pancreatic beta-cells?
• Defective regulatory cell populations in type 1 diabetes
• Host microbiome interactions that alter adaptive immunity in type 1 diabetes
• Novel biomarkers that identify sub-populations of individuals at risk for immune-mediated diabetes
• How T-cell metabolism affects the phenotype of immune function
• Novel therapeutic targets that reboot immune function: from small molecules to CRISP-mediated gene editing
Type 1 diabetes is a general term that describes a condition - usually found in children - which causes immune-mediated pancreatic beta-cell destruction and lifetime insulin use. Claims of a cure around the corner have been made over the past 30 years with little advancement to show for the hundreds of millions of research dollars spent on both basic science experimentation and clinical research trials. In this regard, it is true to say science and medicine slowly evolves and knowledge gaps get filled incrementally over time. Real breakthrough can happen in a moment but is often the culmination of pain staking detailed work, accident, and inspiration.
The 21st century offers science and medicine a cadre of new tools and insights that is enabling us to tackle problems like type 1 diabetes in a highly personalized way with a depth of knowledge previously unachievable. Such areas of knowledge development include the use of gene editing techniques, access to genomic, proteomic, metabolomic, and epigenetic screens that produce large, detailed datasets, and bioinformatic tools that allow these massive datasets to be interrogated and annotated into meaningful information. These new tools are rapidly changing our ability to understand disease states and recognize that our phenotypic description of a disease like type 1 diabetes is a generalization of complex molecular diseases that harbor both meaningful differences and common immunological themes among patients.
The present issue of Frontiers in Immunology will take a bold step towards uncovering our knowledge gaps in the field of type 1 diabetes and describe new approaches to tackling one of our most challenging aspects of human molecular biology, that being an in-depth understanding of alterations in immune function that leads to immune-mediated diabetes.
As we begin to use our new toolbox to fill gaps in knowledge, we can answer questions such as; how pancreatic beta-cell death occurs, what effector cell populations are responsible for beta-cell death, what are the defects in type 1 diabetes regulatory cell populations that allow for a hostile environment, how does the host microbiome interact with the immune system to create a hostile immune environment, and what genetic or epigenetic elements can be manipulated to forestall or prevent disease in susceptible individuals. Equally important, we can learn about new biomarkers and therapeutic targets that might benefit identification of pre-diabetic children who can ultimately have their immune systems re-routed away from their inherent disease trajectory.
This Research Topic welcomes articles focusing on, but not limited to, the following aspects of immune-mediated diabetes:
• Effector cell populations gone awry; how do effector cells kill pancreatic beta-cells?
• Defective regulatory cell populations in type 1 diabetes
• Host microbiome interactions that alter adaptive immunity in type 1 diabetes
• Novel biomarkers that identify sub-populations of individuals at risk for immune-mediated diabetes
• How T-cell metabolism affects the phenotype of immune function
• Novel therapeutic targets that reboot immune function: from small molecules to CRISP-mediated gene editing
