The underlying causes of autoimmune diseases are numerous and often poorly understood. In addition to genetic and lifestyle-related factors, microbes are prominent among the possible environmental triggers of autoimmune processes and proinflammatory pathways. Infectious agents and commensal organisms may initiate cascades, that result in inflammation and possibly improper immune reactions. Alternatively, microbes may play a protective role by favorably modulating proinflammatory pathways. Understanding these mechanisms is essential for designing therapeutic and prophylactic strategies to counteract excessive inflammation and autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, and inflammatory bowel disease.
Infectious agents trigger pro-autoimmune pathways through various mechanisms, such as molecular mimicry, bystander activation, epitope spreading, and cryptic antigen release. For example, antibodies against the Epstein-Barr virus nuclear antigen-1 (EBNA-1) cross-react with the autoantigens Ro, Sm B/B', and Sm D1 associated with lupus. This indicates that EBNA-1 acts as molecular mimic initiating the autoimmune response. However, molecular mechanisms of autoimmune activation employed by microbes are not well delineated in most cases.
More recently, the roles played by commensal microbes be it in protective capacities or as inducers of autoimmunity, have become of particular interest due to the increased usage of microbiota as therapeutic agents.
Hence, the goal of this Research Topic is to shed light on the various mechanisms and molecular processes through which commensal and pathogenic microbes contribute to inflammation and to autoimmune reactions in addition to examining ways by which microbes dampen inflammation or protect against an autoimmune disease.
This Research Topic welcomes the submission of Original Research, Methods, Reviews, Mini-Reviews, Brief Research Reports, Hypothesis and Theory, Perspective, General Commentary, and Opinion-type papers that shed light on mechanisms by which various types of microbes modulate inflammation and pro-autoimmune processes.
Themes within the scope of this Research Topic include, but are not limited to:
• The role of the human microbiome in autoimmunity and inflammation.
• Microbial activation and inhibition of immune cell subsets in autoimmune diseases and inflammatory reactions.
• Cross-reactivity of microbial antigens with host antigens.
• Inflammatory pathway triggering or inhibition by microbial antigens, viral infections or bacterial infections.
• Novel associations between microbial agents and autoimmune diseases that have not been previously described or whose mechanisms have not been examined yet.
• Immunogenetics and microbes in autoimmunity and inflammation.
• Prophylactic approaches or therapeutic agents for inflammatory and autoimmune diseases targeting or involving microbial agents and commensal microbes.
The underlying causes of autoimmune diseases are numerous and often poorly understood. In addition to genetic and lifestyle-related factors, microbes are prominent among the possible environmental triggers of autoimmune processes and proinflammatory pathways. Infectious agents and commensal organisms may initiate cascades, that result in inflammation and possibly improper immune reactions. Alternatively, microbes may play a protective role by favorably modulating proinflammatory pathways. Understanding these mechanisms is essential for designing therapeutic and prophylactic strategies to counteract excessive inflammation and autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, and inflammatory bowel disease.
Infectious agents trigger pro-autoimmune pathways through various mechanisms, such as molecular mimicry, bystander activation, epitope spreading, and cryptic antigen release. For example, antibodies against the Epstein-Barr virus nuclear antigen-1 (EBNA-1) cross-react with the autoantigens Ro, Sm B/B', and Sm D1 associated with lupus. This indicates that EBNA-1 acts as molecular mimic initiating the autoimmune response. However, molecular mechanisms of autoimmune activation employed by microbes are not well delineated in most cases.
More recently, the roles played by commensal microbes be it in protective capacities or as inducers of autoimmunity, have become of particular interest due to the increased usage of microbiota as therapeutic agents.
Hence, the goal of this Research Topic is to shed light on the various mechanisms and molecular processes through which commensal and pathogenic microbes contribute to inflammation and to autoimmune reactions in addition to examining ways by which microbes dampen inflammation or protect against an autoimmune disease.
This Research Topic welcomes the submission of Original Research, Methods, Reviews, Mini-Reviews, Brief Research Reports, Hypothesis and Theory, Perspective, General Commentary, and Opinion-type papers that shed light on mechanisms by which various types of microbes modulate inflammation and pro-autoimmune processes.
Themes within the scope of this Research Topic include, but are not limited to:
• The role of the human microbiome in autoimmunity and inflammation.
• Microbial activation and inhibition of immune cell subsets in autoimmune diseases and inflammatory reactions.
• Cross-reactivity of microbial antigens with host antigens.
• Inflammatory pathway triggering or inhibition by microbial antigens, viral infections or bacterial infections.
• Novel associations between microbial agents and autoimmune diseases that have not been previously described or whose mechanisms have not been examined yet.
• Immunogenetics and microbes in autoimmunity and inflammation.
• Prophylactic approaches or therapeutic agents for inflammatory and autoimmune diseases targeting or involving microbial agents and commensal microbes.
