House dust mite allergens mediate the activation of ckit in dendritic cells via Tolllike receptor 2

Author:              

Publisher: Spandidos Publications

E-ISSN: 1791-3004|12|4|5307-5313

ISSN: 1791-2997

Source: Molecular Medicine Reports, Vol.12, Iss.4, 2015-01, pp. : 5307-5313

Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.

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Abstract

Several studies have demonstrated that the ckit protooncogene and its ligand, stem cell factor, are important in the development of asthma. House dust mite (HDM; Dermatophagoides pteronyssinus) allergens are a major trigger in the development and exacerbation of asthma. HDM allergens can induce the activation of ckit in dendritic cells (DCs), leading to the development of allergic asthma. Previous studies have demonstrated that activation of Tolllike receptor 2 (TLR2) evokes a T helper (Th)2 immune response and promotes experimental asthma. The aim of the present study was to assess whether HDM mediates the activation of ckit in DCs via TLR2. Monocytederived DCs were generated from C57BL/6 mice, and cultured with interleukin (IL)4 and granulocytemacrophage colonystimulating factor. The DCs were then sensitized with HDM (10 µg/ml) for 72 h. TLR2specific small interfering (si)RNA was used to silence and inhibit the expression of TLR2 in the DCs. The expression levels of ckit and B7 (CD80/CD86) were measured, by analyzing the DC culture supernatant for the presence of IL6 and IL12. Inhibition of TLR2 using specific siRNA downregulated the expression of ckit in the HDMactivated DCs. In addition, silencing of TLR2 inhibited the expression of CD80/CD86, decreased the production of IL6, and increased the production of IL12. These results indicated that TRL2 are important in the activation of ckit by HDM in DCs.

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