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Fig. 3 | BMC Gastroenterology

Fig. 3

From: 25(OH) D3 alleviate liver NK cytotoxicity in acute but not in chronic fibrosis model of BALB/c mice due to modulations in vitamin D receptor

Fig. 3

Increased NK 1.1/CD49a + in chronic model is correlated with their dysfunction and low VDR expressions. a. Liver NK 1.1/CD49a + cells showed gradual elevations in proliferations together with the extent of hepatic fibrosis; vitamin D treatments showed further liver NKs recruitments. b. NK 1.1/CD49a + were responsive to vitamin D treatments through increase in their VDR in the WT and acute CCl4 model however were unresponsive in the chronic model. c. NK 1.1/CD49a + showed similar CD107a in the vitamin D untreated mice with further stimulation in the WT and acute model of CCl4. d. NK1.1 cells from the WT and acute model of CCl4 showed to inhibit pHSCs αSMA percentages following co-culture assay following vitamin D treatments. NK1.1 cells from the chronic model of CCl4 showed no effects on αSMA percentages of pHSCs

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