| First Author | Ukah TK | Year | 2021 |
| Journal | Cell Immunol | Volume | 364 |
| Pages | 104360 | PubMed ID | 33866285 |
| Mgi Jnum | J:329702 | Mgi Id | MGI:6824857 |
| Doi | 10.1016/j.cellimm.2021.104360 | Citation | Ukah TK, et al. (2021) Formation of pancreatic beta-cells from precursor cells contributes to the reversal of established type 1 diabetes. Cell Immunol 364:104360 |
| abstractText | Ig-GAD2, an antigen-specific immune modulator, requires bone marrow (BM) cell transfer in order to restore beta (beta)-cell formation and induce recovery from established type 1 diabetes (T1D). The BM cells provide endothelial precursor cells (EPCs) that give rise to islet resident endothelial cells (ECs). This study shows that, during development of T1D, the immune attack causes collateral damage to the islet vascular network. The EPC-derived ECs repair and restore islet blood vessel integrity. In addition, beta-cell genetic tracing indicates that the newly formed beta-cells originate from residual beta-cells that escaped the immune attack and, unexpectedly, from beta-cell precursors. This indicates that the rejuvenated islet microenvironment invigorates formation of new beta-cells not only from residual beta-cells but also from precursor cells. This is twofold significant from the perspective of precursor cells as a safe reserve for restoration of beta-cell mass and its promise for therapy of T1D long after diagnosis. |
