Research Topic

Pathogens, Pathobionts and Autoimmunity

About this Research Topic

The etiology of autoimmune diseases is unknown, but environmental pathogens, commensal organisms, and infectious processes are believed to play roles. Viruses such as Epstein Barr Virus (EBV), Cytomegalovirus (CMV), Human Papillomavirus (HPV) and retroviruses have been associated with autoimmune diseases such as Systemic Lupus Erythematosus (SLE). EBV has also been associated with Rheumatoid Arthritis (RA), Sjogren’s Syndrome (SS) and Multiple Sclerosis (MS). In addition to viruses, bacteria have been linked to autoimmune diseases. Infectious agents and microbiome bacteria, including gut commensals that may translocate to sites outside of the gut and bacteria that form biofilms, have been implicated in autoimmunity. Several mechanisms have been proposed by which microbes can elicit autoimmunity. One mechanism is molecular mimicry. Molecular mimics such as the EBV nuclear antigen 1 (EBNA-1) have been shown to mimic Sm B/B’, Ro60, and dsDNA and are thought to elicit cross-reactive antibodies in SLE and SS. In addition, Ro60 orthologs from commensal bacteria are thought to elicit cross-reactive T-cells and autoantibodies. Another mechanism by which microbes can elicit autoimmunity is by activating specific immune pathways. For instance, amyloid curli protein, a component of biofilms produced by enteric bacteria, can form complexes with dsDNA and stimulate both the innate and adaptive immune systems. Curli can form complexes with dsDNA which can activate dendritic cells via Toll Like Receptor (TLR) 2, causing the release of Type I interferons and curli fibers can induce polyclonal activation of B and T cells thereby accelerating autoimmunity.

In this Research Topic, we would like to examine the role of viral and bacterial pathogens and gut pathobionts in autoimmune disease. The goal is to understand how pathogens and pathobionts can subvert our immune system into responding against self so that we may better design therapeutic strategies that can prevent this from happening.

We especially welcome the submission of Original Research articles, but also Reviews and Clinical Trials, on prevailing and novel mechanisms used by pathogens to elicit SLE and other autoimmune diseases.

Topics will include but are not limited to the following:

- Molecular mimicry by pathogen mimotopes and cross-reactivity of anti-pathogen antibodies and T-cell receptors
- Microbial molecular mimics or activators of specific immune pathways
- Activation of innate receptors such as Toll-receptors and the Aryl hydrocarbon receptor by viruses and bacteria
- Mechanisms of gene-environment interactions in autoimmune disease
- Post-translational modification of autoantigens (e.g. citrullination) induced by specific microbes as triggers of autoimmunity
- Commensal pathobionts that translocate out of the gut as triggers of autoimmunity
- Commensal RNA-binding proteins (e.g. Ro60) orthologs as triggers of autoimmunity
- Bacterial biofilms as triggers of autoimmunity


Keywords: autoimmunity, systemic lupus erythematosus, pathogens, pathobionts, molecular mimicry


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.

The etiology of autoimmune diseases is unknown, but environmental pathogens, commensal organisms, and infectious processes are believed to play roles. Viruses such as Epstein Barr Virus (EBV), Cytomegalovirus (CMV), Human Papillomavirus (HPV) and retroviruses have been associated with autoimmune diseases such as Systemic Lupus Erythematosus (SLE). EBV has also been associated with Rheumatoid Arthritis (RA), Sjogren’s Syndrome (SS) and Multiple Sclerosis (MS). In addition to viruses, bacteria have been linked to autoimmune diseases. Infectious agents and microbiome bacteria, including gut commensals that may translocate to sites outside of the gut and bacteria that form biofilms, have been implicated in autoimmunity. Several mechanisms have been proposed by which microbes can elicit autoimmunity. One mechanism is molecular mimicry. Molecular mimics such as the EBV nuclear antigen 1 (EBNA-1) have been shown to mimic Sm B/B’, Ro60, and dsDNA and are thought to elicit cross-reactive antibodies in SLE and SS. In addition, Ro60 orthologs from commensal bacteria are thought to elicit cross-reactive T-cells and autoantibodies. Another mechanism by which microbes can elicit autoimmunity is by activating specific immune pathways. For instance, amyloid curli protein, a component of biofilms produced by enteric bacteria, can form complexes with dsDNA and stimulate both the innate and adaptive immune systems. Curli can form complexes with dsDNA which can activate dendritic cells via Toll Like Receptor (TLR) 2, causing the release of Type I interferons and curli fibers can induce polyclonal activation of B and T cells thereby accelerating autoimmunity.

In this Research Topic, we would like to examine the role of viral and bacterial pathogens and gut pathobionts in autoimmune disease. The goal is to understand how pathogens and pathobionts can subvert our immune system into responding against self so that we may better design therapeutic strategies that can prevent this from happening.

We especially welcome the submission of Original Research articles, but also Reviews and Clinical Trials, on prevailing and novel mechanisms used by pathogens to elicit SLE and other autoimmune diseases.

Topics will include but are not limited to the following:

- Molecular mimicry by pathogen mimotopes and cross-reactivity of anti-pathogen antibodies and T-cell receptors
- Microbial molecular mimics or activators of specific immune pathways
- Activation of innate receptors such as Toll-receptors and the Aryl hydrocarbon receptor by viruses and bacteria
- Mechanisms of gene-environment interactions in autoimmune disease
- Post-translational modification of autoantigens (e.g. citrullination) induced by specific microbes as triggers of autoimmunity
- Commensal pathobionts that translocate out of the gut as triggers of autoimmunity
- Commensal RNA-binding proteins (e.g. Ro60) orthologs as triggers of autoimmunity
- Bacterial biofilms as triggers of autoimmunity


Keywords: autoimmunity, systemic lupus erythematosus, pathogens, pathobionts, molecular mimicry


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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Submission Deadlines

24 July 2020 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

24 July 2020 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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