| First Author | Huang H | Year | 2021 |
| Journal | Cell Mol Immunol | Volume | 18 |
| Issue | 8 | Pages | 1969-1980 |
| PubMed ID | 32963358 | Mgi Jnum | J:331277 |
| Mgi Id | MGI:7386973 | Doi | 10.1038/s41423-020-00546-y |
| Citation | Huang H, et al. (2021) Liver X receptor beta is required for the survival of single-positive thymocytes by regulating IL-7Ralpha expression. Cell Mol Immunol 18(8):1969-1980 |
| abstractText | Liver X receptors (LXRs) are known as key transcription factors in lipid metabolism and have been reported to play an important role in T-cell proliferation. However, whether LXRs play a role in thymocyte development remains largely unknown. Here, we demonstrated that LXRbeta deficiency caused a reduction in single-positive (SP) thymocytes, whereas the transitions from the double-negative to SP stage were normal. Meanwhile, LXRbeta-null SP thymocytes exhibited increased apoptosis and impairment of the IL-7Ralpha-Bcl2 axis. In addition, the LXR agonist T0901317 promoted the survival of SP thymocytes with enhanced IL-7Ralpha expression in wild-type mice but not in LXRbeta-deficient mice. Mechanistically, LXRbeta positively regulated the expression of IL-7Ralpha via direct binding to the Il7r allele in SP thymocytes, and forced expression of IL-7Ralpha or Bcl2 restored the survival of LXRbeta-defective SP thymocytes. Thus, our results indicate that LXRbeta functions as an important transcription factor upstream of IL-7Ralpha to promote the survival of SP thymocytes. |
