Haichang Huang

Title: Peripheral CD4+ regulatory T cells can be expanded and exhibit suppressive function by low-dose IL-2 stimulation from patients with chronic kidney diseases in vitro
Time: 12:30-13:00


Haichang Huang is a nephrologist at the Kidney Disease Research Center, Jingdong Yumei Kidney Disease Hospital, Beijing, China. He has published several articles in international and national journals

Research Interest


Background: Patients with chronic kidney disease (CKD) often have CD4+ regulatory T cells (Tregs) deficiency or/and dysfunction, leading to chronic inflammation. We aim to investigate the effect, function, and related mechanism of low-dose IL-2 on peripheral blood CD4+ regulatory T cells expansion in vitro from patients with CKD.

Methods: A total of 148 newly diagnosed patients with CKD at stage III and 35 healthy volunteer subjects were recruited into our studies. The number of peripheral Tregs in peripheral blood mononuclear cells isolated from CKD patients, which were characterized by FACS as CD4+CD25hi and CD4+CD25+FoxP3+. The effect of low-dose IL-2 on expansion of Tregs, and the suppressive function of expanded Tregs were also analysized by FACS. The levels of FoxP3 mRNA were detected by qRT-PCR. The activation of IL-2 induced Stat5 and blocking experiments were assessed by Western Blotting and FACS. 

Results: We found that the frequency of peripheral Tregs from CKD patients was significantly lower than that in healthy volunteer subjects. We also showed that IL-2 selectively expanded CD4+CD25hi and CD4+CD25+FoxP3+ regulatory T cells, and also upregulated the expression of FoxP3 mRNA. Our in vitro studies demonstrated that expanded CD4+ regulatory T cells from CKD patients suppressed proinflammatory Th1 and Th17 cell response. Furthermore, STAT5 activation is required for IL-2-induced expansion of regulatory T cells and expression of FoxP3 mRNA from CKD patients.

Conclusions: Our findings support the clinical Treg defects in CKD patients, and the rationale of evaluating low-dose IL-2 treatment for selectively modulating CD4+ Tregs to suppress chronic inflammation.