| First Author | Kanno T | Year | 2024 |
| Journal | Int Immunol | Volume | 36 |
| Issue | 3 | Pages | 129-139 |
| PubMed ID | 38041796 | Mgi Jnum | J:358280 |
| Mgi Id | MGI:7778502 | Doi | 10.1093/intimm/dxad049 |
| Citation | Kanno T, et al. (2024) ACC1-mediated fatty acid biosynthesis intrinsically controls thymic iNKT cell development. Int Immunol 36(3):129-139 |
| abstractText | To meet the energetic requirements associated with activation, proliferation, and survival, T cells switch their metabolic signatures from energetically quiescent to activated. However, little is known about the role of metabolic pathway controlling the development of invariant natural killer T (iNKT) cells. In the present study, we found that acetyl-CoA carboxylase 1 (ACC1), a rate-limiting enzyme for the fatty acid biosynthesis pathway, plays an essential role in the development of iNKT cells in the thymus. Mice lacking T-cell specific ACC1 showed a reduced number of iNKT cells with an increased proportion of iNKT cells at immature stages 0 and 1. Furthermore, mixed bone marrow (BM) chimera experiments revealed that T-cell intrinsic ACC1 expression was selectively important for the development of thymic iNKT cells, especially for the differentiation of the NKT1 cell subset. Our single-cell RNA-sequencing (scRNA-seq) data and functional analysis demonstrated that ACC1 is responsible for survival of developing iNKT cells. Thus, these findings highlighted a novel role of ACC1 in controlling thymic iNKT cell development mediated by the control of cell survival. |
