| First Author | Tai N | Year | 2016 |
| Journal | J Exp Med | Volume | 213 |
| Issue | 10 | Pages | 2129-46 |
| PubMed ID | 27621416 | Mgi Jnum | J:237273 |
| Mgi Id | MGI:5811931 | Doi | 10.1084/jem.20160526 |
| Citation | Tai N, et al. (2016) Microbial antigen mimics activate diabetogenic CD8 T cells in NOD mice. J Exp Med 213(10):2129-46 |
| abstractText | Both animal model and human studies indicate that commensal bacteria may modify type 1 diabetes (T1D) development. However, the underlying mechanisms by which gut microbes could trigger or protect from diabetes are not fully understood, especially the interaction of commensal bacteria with pathogenic CD8 T cells. In this study, using islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-reactive CD8 T cell receptor NY8.3 transgenic nonobese diabetic mice, we demonstrated that MyD88 strongly modulates CD8(+) T cell-mediated T1D development via the gut microbiota. Some microbial protein peptides share significant homology with IGRP. Both the microbial peptide mimic of Fusobacteria and the bacteria directly activate IGRP-specific NY8.3 T cells and promote diabetes development. Thus, we provide evidence of molecular mimicry between microbial antigens and an islet autoantigen and a novel mechanism by which the diabetogenicity of CD8(+) T cells can be regulated by innate immunity and the gut microbiota. |
