Vitamin D3 inhibits micro RNA-17-92 to promote specific immunotherapy in allergic rhinitis

Sci Rep. 2017 Apr 3;7(1):546. doi: 10.1038/s41598-017-00431-1.

Abstract

It is recognized that T helper 2 (Th2) polarization plays a critical role in a large number of immune disorders. Yet, the remedies for reconciling the established Th2 polarization are still limited currently. Published data indicate that micro RNA-17-92 cluster is associated with the skewed immune response; 25 vitamin D3 (VD3) can regulate multiple bioactivities in the body. This study tests a hypothesis that VD3 facilitates the effect of specific immunotherapy (SIT) on Th2 response. We observed that treatment with either SIT or VD3 alleviated AR symptoms as well as reduced serum levels of specific IgE and T helper (Th) 2 cytokines, suppressed miR-19a (one of the members of the miR-17-92 cluster) and increased IL-10 in peripheral B cells, which was further improved in those AR patients treated with both SIT and VD3. The expression of miR-19a and IL-10 was significantly negatively correlated with each other in peripheral B cells of AR patients. Metabolites of VD3 formed a complex with retinoid acid receptor to repress the expression of miR-19a in B cells. We conclude that administration with VD3 promotes the effect of SIT on suppression of AR via repressing the expression of miR-19a in peripheral B cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism
  • Case-Control Studies
  • Cholecalciferol / metabolism*
  • Cytokines / genetics
  • Cytokines / metabolism
  • Female
  • Gene Expression Regulation
  • Humans
  • Immunotherapy
  • Male
  • MicroRNAs / genetics*
  • Middle Aged
  • Multigene Family
  • RNA, Long Noncoding
  • Rhinitis, Allergic / genetics*
  • Rhinitis, Allergic / immunology
  • Rhinitis, Allergic / metabolism*
  • Rhinitis, Allergic / therapy
  • Sublingual Immunotherapy
  • Th2 Cells / immunology
  • Th2 Cells / metabolism
  • Young Adult

Substances

  • Cytokines
  • MIR17HG, human
  • MicroRNAs
  • RNA, Long Noncoding
  • Cholecalciferol