| First Author | Liao W | Year | 2021 |
| Journal | iScience | Volume | 24 |
| Issue | 1 | Pages | 101975 |
| PubMed ID | 33474536 | Mgi Jnum | J:339762 |
| Mgi Id | MGI:6717660 | Doi | 10.1016/j.isci.2020.101975 |
| Citation | Liao W, et al. (2021) The downregulation of IL-18R defines bona fide kidney-resident CD8(+) T cells. iScience 24(1):101975 |
| abstractText | Stepwise induction of CD69 and CD103 marks distinct differentiation stages of mucosal Trms. But the majority of non-mucosal Trm lacks CD103 expression. The expression of CD69 alone cannot faithfully define Trm cells in heavily vascularized non-mucosal tissues, such as the kidney. Here, we found that a subset of kidney Trms downregulated IL-18 receptor during differentiation. Via global transcriptional analysis and parabiosis experiments, we have discovered that the downregulation of interleukin-18 receptor (IL-18R) is associated with the establishment of tissue residency. Together with the expression of CD69, IL-18R(lo) exclusively identify tissue-resident cells whereas IL-18R(hi) population contains both tissue-resident and migratory ones. Local cytokines including transforming growth factor beta (TGF-beta) and interferon alpha (IFN-alpha)/beta as well as TGF-beta-dependent suppression of transcription factor Tcf-1 are essential for IL-18R downregulation during kidney Trm differentiation. Together, we identified a convenient surface marker to distinguish bona fide kidney-resident CD8(+) T cells as well as underlying molecular mechanisms controlling this differentiation process. |
