›› 2015, Vol. 33 ›› Issue (12): 1057-.doi: 10.3969 j.issn.1000-3606.2015.12.014

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Effects of 1,25-dihydroxyvitamin D3 on the stimulating ability of cord blood monocytes-derived dendritic cells to T cells proliferation

LI Haiyuan, TANG Zheng, WANG Yi, SHI Yingying, LIU Zhiwei   

  1. Department of Neonatology, International Peace Maternity and Child Health Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China
  • Received:2015-12-15 Online:2015-12-15 Published:2015-12-15

Abstract:  Objective To explore the effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on the stimulating ability of cord blood monocytes-derived dendritic cells (DCs) to T cells proliferation. Methods Umbilical cord blood was collected in aseptic condition. Cord blood monocytes were isolated and cultured for 8 days in the presence of rhGM-CSF, rhIL-4 and rhTNF-α for inducing to differentiate DCs, then intervened by 1,25(OH)2D3 (10 nmol/L). The expressions of differentiation and maturation markers on dendritic cells were determined by flow cytometry. Mixed lymphocyte reaction (MLR) was used and T cells were stained with CFSE to observe the stimulating ability of DCs to T cells proliferation by flow cytometry. Cytokines in the culture medium of MLR were measured by ELISA. Results 1,25(OH)2D3 treated-DCs stimulated less CD3+ T cells to proliferate than control group (61.6±8.23 vs. 75.21±6.21, P<0.01). Moreover, lower proliferation of both CD3+CD4+ and CD3+CD8+ T cells was observed in intervention group (59.24±10.22 vs. 74.54±6.89, P<0.05; 47.06±12.10 vs 59.97±9.11, P<0.05) . The IL-12 and IFN-γ levels in the culture medium of MLR in intervention group were significantly lower than control group (78.84±11.8 vs .99.06±9.07, P<0.05; 9.76±2.75 vs. 22.45±2.6, P<0.05), however, the IL-4 level in intervention group were significantly higher than control group (49.45±2.84 vs. 35.75±1.89, P<0.01). Conclusions 1,25(OH)2D3 inhibits the capability of DCs to activate CD3+CD4+ and CD3+CD8+ T cells, and instructs DCs to induce Th2 bias.