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Vitamin D regulates immunoglobulin mucin domain molecule‐4 expression in dendritic cells
Author(s) -
Liu Z.Q.,
Li M.G.,
Geng X.R.,
Liu J.,
Yang G.,
Qiu S.Q.,
Liu Z.G.,
Yang P.C.
Publication year - 2017
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/cea.12894
Subject(s) - calcitriol receptor , calcitriol , immunology , antibody , immune system , vitamin d and neurology , biology , dendritic cell , microbiology and biotechnology , medicine , endocrinology
Summary 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.