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Abstract: PO0223

TGF-β-Induced CD8+CD103+ Regulatory T Cells but Not Nature Regulatory T Cells Alleviates Acute Renal Injury Induced by Ischemia-Reperfusion

Session Information

  • AKI Mechanisms - 3
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Xu, Zhenjian, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China
  • Xu, Tongtong, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China
  • Xu, Anping, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China

Acute kidney injury (AKI) is one of the most common complications in clinical practice, inflammatory response induced by hypoxic-reoxygenation is the key mechanism of ischemia-reperfusion acute kidney injury. Regulatory T cells are crucial players in the maintenance of immune homeostasis. Our previous researches show that natural regulatory T cells (nTreg) tend to transfer into Th17 under conditions of inflammation and hypoxia. On the contrary, TGF-b induced CD8+CD103+Treg (CD8+CD103+iTreg), a new subpopulation of iTreg we have identified, maintains stable phenotype and immunomodulatory function. The instability of nTreg under conditions of inflammation and hypoxia suggesting that nTreg are not suitable for treatment of AKI. Accordingly, we studied the role of CD8+CD103+iTreg in alleviating AKI.


In vitro study, we test the phenotype and immunomodulatory function of CD8+CD103+iTreg or nTreg under 1% O2 concentration. In vivo study, CD8+CD103+iTreg(2×106/mouse)or nTreg(2×106/mouse)were injected intravenously daily to the AKI mice from the day of surgery (for 3 days).


The expression of CD103 is stable in CD8+iTreg in vitro under 1% O2 concentration(Fig 1) . nTreg transfer into Th17 under hypoxic condition. However, CD8+CD103+iTreg seldom transfer into Th17, remain Foxp3 under hypoxic condition (Fig 2,3). In addition, the suppressive function of CD8+CD103+iTreg over T cells proliferation under hypoxia remain steadily. In vivo study, we found that CD8+CD103+iTreg ameliorate the development of AKI by decreasing the level of serum creatine, alleviating acute tubular necrosis (ATN) and reducing the mortality of AKI mice. (Fig 4).


CD8+CD103+iTreg maintains stable phenotype and immunomodulatory function under condition of hypoxia, decrease the severity of AKI induced by ischemia-reperfusion. CD8+CD103+iTreg provide a promising approach for the treatment of AKI.