Z-Q Liu1,2,3, M-G Li1, X-R Geng1,2,3, J Liu4, G Yang1,2,3, S-Q Qiu2, Z-G Liu1, P-C Yang1. 1. ENT Institute of the Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen, China. 2. Longgang ENT Hospital and Shenzhen ENT Institute, Shenzhen, China. 3. The Brain Body Institute, McMaster University, Hamilton, ON, Canada. 4. Shenzhen Maternity & Child Health Hospital, Shenzhen, China.
Abstract
BACKGROUND: Dendritic cell (DC)-derived immunoglobulin domain molecule (TIM)4 plays a critical role in the initiation of T helper (Th)2 polarization. Vitamin D (VitD) involves the regulation of a number of immune responses. OBJECTIVES: This study tests a hypothesis that VitD regulates TIM4 expression in DCs. METHODS: Peripheral blood samples were collected from patients with allergic rhinitis (AR) and healthy subjects. DCs were isolated from the samples and analyzed for the expression of TIM4. RESULTS: We observed that the levels of calcitriol, the active form of VitD3, in the sera of AR patients were lower than that in healthy subjects. The peripheral DC expressed higher levels of TIM4 and lower levels of VDR. A negative correlation was identified between the data of serum calcitriol and TIM4 in DCs. Exposure DCs to calcitriol in the culture increased the expression of VDR. We also found that VDR bound to the TIM4 promoter locus in DCs to repress the TIM4 gene transcription and expression. CONCLUSIONS AND CLINICAL RELEVANCE: VitD deficiency may contribute to the pathogenesis of AR by increasing the TIM4 expression. The results suggest that to regulate the serum calcitriol levels and the expression of VDR in DCs may be necessary to be taken into account in the treatment of AR.
BACKGROUND: Dendritic cell (DC)-derived immunoglobulin domain molecule (TIM)4 plays a critical role in the initiation of T helper (Th)2 polarization. Vitamin D (VitD) involves the regulation of a number of immune responses. OBJECTIVES: This study tests a hypothesis that VitD regulates TIM4 expression in DCs. METHODS: Peripheral blood samples were collected from patients with allergic rhinitis (AR) and healthy subjects. DCs were isolated from the samples and analyzed for the expression of TIM4. RESULTS: We observed that the levels of calcitriol, the active form of VitD3, in the sera of AR patients were lower than that in healthy subjects. The peripheral DC expressed higher levels of TIM4 and lower levels of VDR. A negative correlation was identified between the data of serum calcitriol and TIM4 in DCs. Exposure DCs to calcitriol in the culture increased the expression of VDR. We also found that VDR bound to the TIM4 promoter locus in DCs to repress the TIM4 gene transcription and expression. CONCLUSIONS AND CLINICAL RELEVANCE: VitD deficiency may contribute to the pathogenesis of AR by increasing the TIM4 expression. The results suggest that to regulate the serum calcitriol levels and the expression of VDR in DCs may be necessary to be taken into account in the treatment of AR.