| Literature DB >> 30260469 |
H Huang1, J-Y Hong2, Y-J Wu2,3, E-Y Wang2, Z-Q Liu2,3,4, B-H Cheng2,3, L Mei1, Z-G Liu2, P-C Yang1,2, P-Y Zheng1.
Abstract
Vitamin D receptor (VDR) mediates various biochemical activities between the cytoplasm and the nucleus in the cell. The nucleotide-binding, oligomerization domain (NOD)-like receptor family, pyrin domain containing 3 (NLRP3) protein is involved in the T helper type 2 (Th2) response. This study tests a hypothesis that VDR interacts with NLRP3 to restrict the Th2-biased response. In this study, VDR-/- mice and WT (WT) mice were used. Th2 cell differentiation between VDR-/- mice and WT mice was observed. We observed that CD4+ T cell activation was higher in VDR-/- mice. The VDR-/-CD4+ T cells were prone to Th2 polarization. VDR-/- mice produced more immunoglobulin (Ig)E. VDR bound NLRP3 to prevent Th2 differentiation by restricting IL4 gene transcription. Th2 biased inflammation spontaneously developed in the intestine of VDR-/- mice. In conclusion, VDR binds NLRP3 to restrict IL4 gene transcription and prevent biased Th2 polarization.Entities:
Keywords: T helper cell; T lymphocyte; Th2 polarization; allergy; vitamin D receptor
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Year: 2018 PMID: 30260469 PMCID: PMC6156809 DOI: 10.1111/cei.13164
Source DB: PubMed Journal: Clin Exp Immunol ISSN: 0009-9104 Impact factor: 4.330