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.
Highlights
In some predisposed individuals, harmless foreign substances, such as inhaled particles, airborne pollens, may trigger aberrant immune responses and cause immune inflammations in the local tissue such as airway allergy
To investigate the mechanism by which administration with vitamin D3 (VD3) facilitates the therapeutic efficacy of specific immunotherapy (SIT), we evaluated the regulatory effect of VD3 on the expression of a miR-17-92 cluster in peripheral B cells in allergic rhinitis (AR) patients based on published data that miR-17-92 cluster plays an important role in promoting T helper 2 (Th2) polarization[6]
The results showed a complex of calcitriol/VD receptor (VDR)/retinoid acid X receptor (RXR) (CVR) in the B cells collected at month 6 (Fig. 6A)
Summary
Harmless foreign substances, such as inhaled particles, airborne pollens, may trigger aberrant immune responses and cause immune inflammations in the local tissue such as airway allergy. MiRNAs are found in plants and animals involved in post-transcriptional regulation of gene expression. Elevated expression of miR17-92 has been observed in a variety of immune disorders, such as cancer[5] and allergic asthma[6]. Whether the regulation of the miR-17-92 cluster is involved in the effect of VD3 on suppression of immune inflammation has not been investigated. Specific immunotherapy (SIT), known as “desensitization” or “hypo-sensitization”, is a medical therapy for allergic diseases[10]. The effects of SIT include attenuation of allergic symptoms, generation of tolerant immune cells, induction of blocking antibodies such as IgG411. Based on the information above, we hypothesize that the therapeutic effect of SIT can be strengthened by VD3 via regulating the expression of a miR-17-92 cluster. The addition of VD3 significantly enhanced the therapeutic effect of SIT on AR symptoms
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