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https://www.selleckchem.com/products/adt-007.html 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. A 16-year-old patient seen in the Emergency Department due to loss of visual acuity (VA) in the left eye (LE), and oppressive headache of 1 day onset. The patient was on treatment with topical corticosteroids for viral conjunctivitis. The VA was 1.00 in the right eye and 0.05 in LE. The intraocular pressure was 42mmHg in both eyes. In the LE, the funduscopy revealed retinal ischaemic oedema in the papillomacular bundle. The optical coherence tomography angiography (OCT-A) showed an obstruction of the cilioretinal artery. The systemic study was normal, the cardiac and supra-aortic trunks ultrasound was normal, with ocular hyperte

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