| First Author | Park JG | Year | 2020 |
| Journal | Kidney Int | Volume | 97 |
| Issue | 5 | Pages | 980-994 |
| PubMed ID | 32143848 | Mgi Jnum | J:341675 |
| Mgi Id | MGI:7541699 | Doi | 10.1016/j.kint.2019.11.025 |
| Citation | Park JG, et al. (2020) Kidney residency of VISTA-positive macrophages accelerates repair from ischemic injury. Kidney Int 97(5):980-994 |
| abstractText | Tissue-resident macrophages have unique tissue-specific functions in maintaining homeostasis and resolving inflammation. However, the repair role and relevant molecules of kidney-resident macrophages after ischemic injury remain unresolved. To this end, mice without kidney-resident R1 macrophages but containing infiltrating monocyte-derived R2 macrophages were generated using differential cellular kinetics following clodronate liposome treatment. When ischemia-reperfusion injury was induced in these mice, late phase repair was reduced. Transcriptomic and flow cytometric analyses identified that V-domain Ig suppressor of T cell activation (VISTA), an inhibitory immune checkpoint molecule, was constitutively expressed in kidney-resident R1 macrophages, but not in other tissue-resident macrophages. Here, VISTA functioned as a scavenger of apoptotic cells and served as a checkpoint to control kidney-infiltrating T cells upon T cell receptor-mediated stimulation. Together these functions improved the repair process after ischemia-reperfusion injury. CD14(+) CD33(+) mononuclear phagocytes of human kidney also expressed VISTA, which has similar functions to the mouse counterpart. Thus, VISTA is upregulated in kidney macrophages in a tissue-dependent manner and plays a repair role during ischemic injury. |
