ArticleCell death & disease2026
CXCR6+ T cells promote apoptosis and necroptosis in proximal tubules during AKI-to-CKD transition.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute kidney injury (AKI) can progress to chronic kidney disease (CKD) in the setting of maladaptive repair characterized by tubular atrophy, inflammation, and fibrosis. Programmed cell death is a key driver of proximal tubule (PT) loss, yet how immune infiltration promotes tubular injury and death remains incompletely understood. Using a mouse model of maladaptive repair, we integrated bulk and single-cell RNA sequencing with immunohistochemistry and protein analyses to define immune-epithelial interactions during AKI-to-CKD transition. Injured kidneys exhibited loss of healthy PTs, expansion of injured PT subsets, and late-stage T cell accumulation. Apoptotic and necroptotic signaling pathways were markedly upregulated, particularly in VCAM1+ PT cells. Cell-cell interaction analysis identified macrophage-derived Cxcl16 as the dominant chemokine mediating recruitment of Cxcr6+ T cells. Genetic deletion of Cxcr6 reduced renal T cell accumulation, cytotoxic effector expression, and activation of apoptotic (cleaved caspase-3, Bax) and necroptotic signaling (MLKL, phospho-MLKL) in PT cells. Accordingly, Cxcr6
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