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Editorial
. 2019 Jan;195(1):10-14.
doi: 10.1111/cei.13239.

Pathogen infection and autoimmune disease

U Christen  1
Affiliations
Editorial

Pathogen infection and autoimmune disease

U Christen. Clin Exp Immunol. 2019 Jan.
No abstract available

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Figures

Figure 1
Figure 1
Impact of pathogens on autoimmunity. Several mechanisms have been suggested how pathogens might be involved in the initiation or acceleration of autoimmune diseases (left) or how they might decelerate an ongoing autoimmune process or even protect from autoimmune disease (right). This figure provides a schematic overview of some of them without claiming to be complete. Initiation/acceleration: pathogens can cause direct damage to infected cells (1) leading to necrosis or initiate a necroptosis programme in infected cells (2). The infection‐associated release of a plethora of inflammatory mediators may trigger bystander activation (3), including the up‐regulation of major histocompatibility complex (MHC) molecules, resulting in an enhanced presentation of pathogen and host peptides. Pathogen‐derived superantigens, such as staphylococcal enterotoxins, may cross‐link MHC molecules directly with the T cell receptor (TCR) without requiring a specific peptide (4), resulting in a polyclonal T cell activation. Molecular mimicry between pathogen and host (5) might activate pathogen‐specific lymphocytes that also cross‐react to self‐antigens. Both direct damage and determinant epitope spreading might result in the exposure of cryptic or previously sequestered epitopes (6) to which no tolerance had been established. Protection/deceleration: pathogens, particularly parasites, can induce an immune balance shift towards a type 2 (Th2/Tc2) response (7). Immunomodulatory cytokines and other suppressive factors may induce tolerogenic dendritic cells and/or bystander regulatory T cells (8). Pathogen infection at a remote location might cause a deviation (9) for aggressive cells that might follow a stronger chemokine gradient leading away from the site of autoimmune destruction. Finally, pathogens might induce target autoantigen‐specific regulatory T cells. Note that additional factors, including genetic predisposition, microbiome and others, impact the outcome of the autoimmune process.
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References

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