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<p>Activated immune cells infiltrate the vasculature during the pathophysiology of hypertension by establishing a vascular-immune interface that contributes to blood pressure dysregulation and organ failure. Many observations indicate a key role of CD8<sup>+</sup> T cells in hypertension but mechanisms regulating their activation and interplay with the cardiovascular system are still unknown. In murine model, here we show that a specific member of the phosphoinositide-3-kinases (PI3K) family of lipid kinases, PI3Kγ, is a key intracellular signaling of CD8<sup>+</sup> T cells activation and RANTES/CCL5 secretion in hypertension: CCL5-CCR5 signaling is crucial for the establishment of the vascular-immune interface in peripheral organs, lastly contributing to CD8<sup>+</sup> tissue infiltration, organ dysfunction and blood pressure elevation. Our studies identify PI3Kγ as a booster of effector CD8<sup>+</sup> T cell function, even in the absence of external stimuli. Lastly, an enhanced PI3Kγ signaling mediates the bystander activation of CD8<sup>+</sup> T cells and proves effective in transferring the hypertensive phenotype between mice.</p>

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PI3Kγ signaling controls trafficking of CD8+ T cells between lymphoid and non-lymphoid organs and drives hypertension in a murine model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月1日

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  • Marialuisa Perrotta,
  • Sara Perrotta,
  • Lorenzo Carnevale,
  • Agnese Migliaccio,
  • Fabio Pallante,
  • Ryszard Nosalski,
  • Tomasz J. Guzik,
  • Stefania Fardella,
  • Emilio Hirsch,
  • Valentina Fardella,
  • Azzurra Zonfrilli,
  • Jacopo Pacella,
  • Matthias P. Wymann,
  • Giuseppe Lembo,
  • Daniela Carnevale

摘要

Activated immune cells infiltrate the vasculature during the pathophysiology of hypertension by establishing a vascular-immune interface that contributes to blood pressure dysregulation and organ failure. Many observations indicate a key role of CD8+ T cells in hypertension but mechanisms regulating their activation and interplay with the cardiovascular system are still unknown. In murine model, here we show that a specific member of the phosphoinositide-3-kinases (PI3K) family of lipid kinases, PI3Kγ, is a key intracellular signaling of CD8+ T cells activation and RANTES/CCL5 secretion in hypertension: CCL5-CCR5 signaling is crucial for the establishment of the vascular-immune interface in peripheral organs, lastly contributing to CD8+ tissue infiltration, organ dysfunction and blood pressure elevation. Our studies identify PI3Kγ as a booster of effector CD8+ T cell function, even in the absence of external stimuli. Lastly, an enhanced PI3Kγ signaling mediates the bystander activation of CD8+ T cells and proves effective in transferring the hypertensive phenotype between mice.