ArticleImmunologic research2013
House dust mite allergen Der f 2 induces interleukin-13 expression by activating the PI3K/Akt pathway.
Article in Immunologic research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Crucial role of stimulator of interferon genes-dependent signaling in house dust mite extract-induced IgE production.Scientific reports · 2021Article
- ADRB2 suppresses IL-13-induced allergic rhinitis inflammatory cytokine regulated by miR-15a-5p.Human cell · 2019Article
- MicroRNA 27b-3p Modulates SYK in Pediatric Asthma Induced by Dust Mites.Frontiers in pediatrics · 2018Article
- Regulation of CBL and ESR1 expression by microRNA-22‑3p, 513a-5p and 625-5p may impact the pathogenesis of dust mite-induced pediatric asthma.International journal of molecular medicine · 2016Article
- The Deubiquitinase USP17 Regulates the Stability and Nuclear Function of IL-33.International journal of molecular sciences · 2015Article
- Influence of the Adjuvants and Genetic Background on the Asthma Model Using Recombinant Der f 2 in Mice.Immune network · 2013Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
House dust mites (HDMs) are a common cause of allergic asthma. The group 2 allergen from Dermatophagoides farinae, Der f 2, is one of the major HDM allergens. Elevated Der f 2 immunoglobulin E (IgE) levels are observed in most of the allergic patients. Interleukin-13 (IL-13), a gene associated with asthma pathology, was induced by Der f 2 in BEAS-2B human airway epithelial cells; however, the signaling pathways associated with Der f 2 are not fully understood. In this study, we identified a role of the phosphatidylinositol-3-kinase (PI3K)/Akt pathway, a well-known potential target for anti-asthma drugs, in the IL-13 induction by Der f 2. First, Der f 2 activated the PI3K/Akt pathway, which subsequently activated the nuclear factor-kappa B (NF-κB) pathway and induced IL-13 expression in BEAS-2B cells. Treatment with the PI3K inhibitor LY294002 abolished Der f 2-induced activation of Akt and NF-κB and the expression of IL-13. Furthermore, Der f 2-induced activation of the PI3K/Akt and NF-κB pathways, expression of IL-13, and the blockade of these effects with a PI3K inhibitor were confirmed in the lungs of mice that were intranasally exposed to Der f 2. Taken together, these results indicate that the PI3K/Akt pathway regulates Der f 2-induced IL-13 expression via activation of the NF-κB pathway.
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