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On the other hand, complicated microbial antigens and enormous amount of microbial metabolites may trigger autoimmune diseases [3].
Low avidity autoreactive CD8+ T cells can escape both central and peripheral tolerance and may trigger autoimmune reactions to a microbial mimic of self-antigen [ 38].
The fact that they are also present at regions containing immune system components and an inflammatory milieu has led to increasing evidence that NETs may trigger autoimmune responses.
Increasing evidence suggests that environmental factors, including epigenetic DNA methylation, chemical exposures, and host-pathogen interactions, may trigger autoimmune conditions in genetically susceptible individuals [ 3- 5].
Moreover, repeated episodes of GAS infection may trigger autoimmune diseases such as acute post-streptococcal glomerulonephritis and acute rheumatic fever (ARF).
Furthermore, environmental factors (Epstein-bar virus and pesticides) and hormones may trigger autoimmune responses and modulate the alternating periods of SLE flares [ 14].
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Even though the virus may not trigger autoimmune disease, it may be reactivated by an initial inflammatory insult and thereafter sustain and exacerbate inflammatory processes by producing type I cytokines and by specific mechanisms that induce inflammation and autoimmune reactions.
Viral infection of such as HCV may thus possibly trigger autoimmune hepatitis.
It is postulated that previously restricted epitopes are exposed by statins and this may trigger an autoimmune myopathy.
It is generally observed that exogenous antigens may trigger an autoimmune peripheral demyelination by a molecular mimicry-induced loss of tolerance.
It would not be surprising if the production of anti-TIF1β is also linked with cancer-associated DM as overexpression and modification of self-protein may trigger an autoimmune response.
More suggestions(15)
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