| First Author | Li Y | Year | 2021 |
| Journal | Mol Immunol | Volume | 139 |
| Pages | 131-138 | PubMed ID | 34482201 |
| Mgi Jnum | J:312972 | Mgi Id | MGI:6792560 |
| Doi | 10.1016/j.molimm.2021.08.022 | Citation | Li Y, et al. (2021) Deficiency in WDFY4 reduces the number of CD8(+) T cells via reactive oxygen species-induced apoptosis. Mol Immunol 139:131-138 |
| abstractText | WDFY4 (WD repeat and FYVE domain-containing 4) is a susceptibility gene involved in several autoimmune diseases and plays an important role in the immune system. However, it is not clear how WDFY4 affects T cells. We have generated a Wdfy4-knockout mouse and found that selective deficiency of Wdfy4 in T cells led to a reduction in the number of CD8(+) T cells in the periphery, thus promoting tumor growth when mice were challenged with a transplantable tumor. Moreover, conditional ablation of Wdfy4 in T cells enhanced the apoptosis of CD8(+) T cells and increased the intracellular levels of reactive oxygen species accompanied by the upregulation of Nox2. Mechanistically, the decrease in the CD8(+) T-cell numbers in Wdfy4-knockout mice was associated with activation of the p53 pathway and inhibition of the extracellular signal-regulated kinase pathway. In addition, WDFY4 participated in cell proliferation. In conclusion, our results elucidate the biological role of WDFY4 in apoptosis and establish a link between WDFY4 and T cells. |
