| First Author | Wan X | Year | 2016 |
| Journal | J Exp Med | Volume | 213 |
| Issue | 6 | Pages | 967-78 |
| PubMed ID | 27139492 | Mgi Jnum | J:232772 |
| Mgi Id | MGI:5780148 | Doi | 10.1084/jem.20151869 |
| Citation | Wan X, et al. (2016) Class-switched anti-insulin antibodies originate from unconventional antigen presentation in multiple lymphoid sites. J Exp Med 213(6):967-78 |
| abstractText | Autoantibodies to insulin are a harbinger of autoimmunity in type 1 diabetes in humans and in non-obese diabetic mice. To understand the genesis of these autoantibodies, we investigated the interactions of insulin-specific T and B lymphocytes using T cell and B cell receptor transgenic mice. We found spontaneous anti-insulin germinal center (GC) formation throughout lymphoid tissues with GC B cells binding insulin. Moreover, because of the nature of the insulin epitope recognized by the T cells, it was evident that GC B cells presented a broader repertoire of insulin epitopes. Such broader recognition was reproduced by activating naive B cells ex vivo with a combination of CD40 ligand and interleukin 4. Thus, insulin immunoreactivity extends beyond the pancreatic lymph node-islets of Langerhans axis and indicates that circulating insulin, despite its very low levels, can have an influence on diabetogenesis. |
