Genetic Basis of Tolerance Induction Defects Underlying the Development of Autoimmune Pathologies

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Background

Frontiers in Immunology (FI) is issuing a call for the submission of articles centered on the genetic basis of tolerance induction defects underlying the development of autoimmune pathologies. Most autoimmune diseases are under complex polygenic control. However, there is evidence that some allelic variants can contribute to multiple autoimmune diseases. whereas some genetic variants uniquely contribute to a specific autoimmune disease. It has also been found that gene variants may alter responses to various possible therapeutic agents, changing disease outcomes.

There has been controversy concerning how well some animal models, in particular mice, inform the basis of various autoimmune pathologies in humans. Thus, more investigation is needed to ascertain potential similarities or differences in gene variants contributing to causative tolerance induction defects in human patients and various animal models. Another consideration is that gene variants contributing to a particular autoimmune disease state in humans and a particular animal model may not be identical but might have some similarities in terms of the shared biochemical network disrupted, leading to a failure of tolerance induction.

It has been long known that regulatory T-cells (Tregs) play an important role in maintaining peripheral tolerance, and hence gene variants that disrupt their development or activity can result in autoimmune disease states. Thus, it is important to review the genetic control of Treg development. However, it is now becoming increasingly appreciated there is also a subset of regulatory B-cells (Bregs) that contribute to the prevention of autoimmunity and less is known about the genetic control of the development and activity of Bregs than Tregs. For this reason, it is important that we understand the relative contributions of Treg and Breg development and activity and how this might relate to susceptibility or resistance to various autoimmune diseases.

The incidence of various autoimmune diseases has significantly increased in recent decades. This indicates relatively recent environmental changes intersect with genetic factors to influence susceptibility to autoimmunity. Thus, a greater understanding of how autoimmunity can be caused by the changing dynamic of interactions between genes with the environment could be significant. Some autoimmune diseases such as type 1 diabetes (T1D), if left untreated, would often result in lethality at a young pre-reproductive age and so studies on how these genes survived from a evolutionary standpoint would be welcome.

This Research Topic will explore the genetic basis of how tolerance induction defects underlie autoimmunity. We welcome articles focusing on, but not limited, the following sub-topics:

• The genetic basis for tolerance induction defects underlying any single or multiple autoimmune disease states
• How gene variants may alter responses to various possible therapeutic agents
• The potential similarities or differences in gene variants contributing to causative tolerance induction defects in human patients and various animal models
• How gene variants might disrupt a shared biochemical network essential to tolerance induction across human and animal models
• The genetic control of Treg development/activity
• Recent findings on the genetic control of Breg development and activity, and how this may contribute to susceptibility or resistance to various autoimmune diseases
• A comparison of the genetic basis of Treg and Breg development.
• How genes environmental interactions contribute to various autoimmune states
• Why “autoimmunity genes” have not been eliminated by natural selection

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.

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