| First Author | Dang AT | Year | 2021 |
| Journal | iScience | Volume | 24 |
| Issue | 1 | Pages | 101900 |
| PubMed ID | 33364588 | Mgi Jnum | J:338665 |
| Mgi Id | MGI:6819416 | Doi | 10.1016/j.isci.2020.101900 |
| Citation | Dang AT, et al. (2021) NLRC5 promotes transcription of BTN3A1-3 genes and Vgamma9Vdelta2 T cell-mediated killing. iScience 24(1):101900 |
| abstractText | BTN3A molecules-BTN3A1 in particular-emerged as important mediators of Vgamma9Vdelta2 T cell activation by phosphoantigens. These metabolites can originate from infections, e.g. with Mycobacterium tuberculosis, or by alterations in cellular metabolism. Despite the growing interest in the BTN3A genes and their high expression in immune cells and various cancers, little is known about their transcriptional regulation. Here we show that these genes are induced by NLRC5, a regulator of MHC class I gene transcription, through an atypical regulatory motif found in their promoters. Accordingly, a robust correlation between NLRC5 and BTN3A gene expression was found in healthy, in M. tuberculosis-infected donors' blood cells, and in primary tumors. Moreover, forcing NLRC5 expression promoted Vgamma9Vdelta2 T-cell-mediated killing of tumor cells in a BTN3A-dependent manner. Altogether, these findings indicate that NLRC5 regulates the expression of BTN3A genes and hence open opportunities to modulate antimicrobial and anticancer immunity. |
