Abstract
In addition to genetic predisposition, environmental determinants contribute to a complex etiology leading to onset of type 1 diabetes (T1D). Multiple studies have established the gut as an important site for immune modulation that can directly impact development of autoreactive cell populations against pancreatic self-antigens. Significant efforts have been made to unravel how changes in the microbiome function as a contributor to autoimmune responses and can serve as a biomarker for diabetes development. Large-scale longitudinal studies reveal that common environmental exposures precede diabetes pathology. Virus infections, particularly those associated with the gut, have been prominently identified as risk factors for T1D development. Evidence suggests recent-onset T1D patients experience pre-existing subclinical enteropathy and dysbiosis leading up to development of diabetes. The start of these dysbiotic events coincide with detection of virus infections. Thus viral infection may be a contributing driver for microbiome dysbiosis and disruption of intestinal homeostasis prior to T1D onset. Ultimately, understanding the cross-talk between viral infection, the microbiome, and the immune system is key for the development of preventative measures against T1D.
Highlights
Type 1 diabetes (T1D) is a persistent autoimmune disorder where immune cells attack and destroy the insulin-producing beta cells of the pancreas
This review primarily focuses on the impact of commensal bacterial communities and later the collective virome
This study found that the mice developed impaired mucin production, dysbiosis, modified secretion of bacteria-specific IgA, and alterations in lamina propria dendritic and T cell populations – which skew toward an inflammatory rather than regulatory profile
Summary
Type 1 diabetes (T1D) is a persistent autoimmune disorder where immune cells attack and destroy the insulin-producing beta cells of the pancreas. The authors showed that MAIT celldeficient (MR1-restricted) NOD mice have increased rates of diabetes and have a modified gut mucosal environment – suggesting that they can be protective [97] Beyond their role in sensing bacterial products, MAIT cells have been identified to hold potent inflammatory responses in both acute and chronic virus infections [98]. This subsequent loss of intestinal integrity can induce activation of islet-specific immune cells in the gut to travel to the pancreas and promote onset of diabetes in T cell receptor-transgenic BDC2.5 crossed NOD mice Activation of these T cells appeared to be dependent on the presence of the gut microbiome; microbial dysbiosis caused by the DSStreatment alone was not sufficient to promote autoimmunity. Researchers have observed the intestinal virome dramatically shifting prior to onset of T1D
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