| First Author | Huang Q | Year | 2020 |
| Journal | EMBO Mol Med | Volume | 12 |
| Issue | 11 | Pages | e12305 |
| PubMed ID | 33034128 | Mgi Jnum | J:348448 |
| Mgi Id | MGI:6799805 | Doi | 10.15252/emmm.202012305 |
| Citation | Huang Q, et al. (2020) IL-10 producing type 2 innate lymphoid cells prolong islet allograft survival. EMBO Mol Med 12(11):e12305 |
| abstractText | Type 2 innate lymphoid cells (ILC2s) are a subset of ILCs with critical roles in immunoregulation. However, the possible role of ILC2s as immunotherapy against allograft rejection remains unclear. Here, we show that IL-33 significantly prolonged islet allograft survival. IL-33-treated mice had elevated numbers of ILC2s and regulatory T cells (Tregs). Depletion of Tregs partially abolished the protective effect of IL-33 on allograft survival, and additional ILC2 depletion in Treg-depleted DEREG mice completely abolished the protective effects of IL-33, indicating that ILC2s play critical roles in IL-33-mediated islet graft protection. Two subsets of ILC2s were identified in islet allografts of IL-33-treated mice: IL-10 producing ILC2s (ILC2(10) ) and non-IL-10 producing ILC2s (non-ILC(10) ). Intravenous transfer of ILC2(10) cells, but not non-ILC(10) , prolonged islet allograft survival in an IL-10-dependent manner. Locally transferred ILC2(10) cells led to long-term islet graft survival, suggesting that ILC2(10) cells are required within the allograft for maximal suppressive effect and graft protection. This study has uncovered a major protective role of ILC2(10) in islet transplantation which could be potentiated as a therapeutic strategy. |
