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Publication : Kidney residency of VISTA-positive macrophages accelerates repair from ischemic injury.

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.
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