| First Author | Li YY | Year | 2017 |
| Journal | J Autoimmun | Volume | 82 |
| Pages | 85-95 | PubMed ID | 28592385 |
| Mgi Jnum | J:272790 | Mgi Id | MGI:6282415 |
| Doi | 10.1016/j.jaut.2017.05.007 | Citation | Li YY, et al. (2017) Nucleotide-binding oligomerization domain-containing protein 2 (Nod2) modulates T1DM susceptibility by gut microbiota. J Autoimmun 82:85-95 |
| abstractText | Nucleotide-binding oligomerization domain-containing protein 2 (Nod2) is an innate immune receptor. To investigate the role of Nod2 in susceptibility to the autoimmune disease, type 1 diabetes mellitus (T1DM), we generated Nod2(-/-) non-obese diabetic (NOD) mice. The Nod2(-/-)NOD mice had different composition of the gut microbiota compared to Nod2(+/+)NOD mice and were significantly protected from diabetes, but only when housed separately from Nod2(+/+)NOD mice. This suggested that T1DM susceptibility in Nod2(-/-)NOD mice is dependent on the alteration of gut microbiota, which modulated the frequency and function of IgA-secreting B-cells and IL-10 promoting T-regulatory cells. Finally, colonizing germ-free NOD mice with Nod2(-/-)NOD gut microbiota significantly reduced pro-inflammatory cytokine-secreting immune cells but increased T-regulatory cells. Thus, gut microbiota modulate the immune system and T1D susceptibility. Importantly, our study raises a critical question about the housing mode in the interpretation of the disease phenotype of genetically-modified mouse strains in T1DM studies. |
