Journal
ONCOTARGET
Volume 7, Issue 1, Pages 148-160Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.6653
Keywords
allergic rhinitis; BCTC; CD4 T lymphocyte; OVA; TRPV1; Immunology and Microbiology Section; Immune response; Immunity
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Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [NRF2013R1A1A4A01010519]
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Transient receptor potential vanilloid 1 (TRPV1), which has been identified as a molecular target for the activation of sensory neurons by various painful stimuli, was reported to regulate the signaling and activation of CD4(+) T cells. However, the role of TRPV1 in CD4(+) T cell in allergic rhinitis remains poorly understood. In this study, TRPV1 expression was localized in CD4(+) T cells. Both knockout and chemical inhibition of TRPV1 suppressed Th2/Th17 cytokine production in CD4 T cells and Jurkat T cells, respectively, and can suppress T cell receptor signaling pathways including NF-kappa B, MAP kinase, and NFAT. In TRPV1 knockout allergic rhinitis (AR) mice, eosinophil infiltration, Th2/Th17 cytokines in the nasal mucosa, and total and ova-specific IgE levels in serum decreased, compared with wild-type AR mice. The TRPV1 antagonists, BCTC or theobromine, showed similar inhibitory immunologic effects on AR mice models. In addition, the number of TRPV1(+)/CD4(+) inflammatory cells increased in the nasal mucosa of patients with AR, compared with that of control subjects. Thus, TRPV1 activation on CD4(+) T cells is involved in T cell receptor signaling, and it could be a novel therapeutic target in AR.
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