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Kidney Week

Abstract: FR-PO093

Kidney Residency of VISTA-Positive Macrophages Accelerates Repair from Ischemic Injury

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Han, Seung Seok, Seoul National University College of Medicine, Seoul, Korea (the Republic of)
  • Kim, Dong Ki, Seoul National University Hospital, Seoul, Korea (the Republic of)
  • Yang, Seung Hee, Kidney Research Institute, Seoul National University, Seoul, Korea (the Republic of)
Background

V-domain Ig suppressor of T cell activation (VISTA), expressed primarily in myeloid cells, promotes the progression of cancer via acting as an inhibitory immune-checkpoint molecule. Nevertheless, the VISTA-dependent role of tissue myeloid cells within the normal organ environment remains unresolved.

Methods

VISTA expression was analyzed in homeostatic condition and compared between tissues. To address the role of VISTA, we adopted ischemia-reperfusion injury. Human renal mononuclear phagocytes were used to translate the mouse results to the human condition.

Results

In contrast to lung, liver, and skin, the renal residency of macrophages highly expressed VISTA in ischemic injury as well as homeostasis. When these kidney-resident macrophages were predominantly depleted, the repair from ischemic injury was hindered. 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. All of these functions eventually improved the repair process after ischemic injury. CD14+ CD33+ mononuclear phagocytes of human kidney also expressed VISTA, which had similar functions to the mouse counterpart.

Conclusion

VISTA is upregulated in kidney macrophages in a tissue-dependent manner, which plays a repair role from ischemic injury.