Research Papers: Immunology:
The role of TRPV1 in the CD4+ T cell-mediated inflammatory response of allergic rhinitis
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Ramachandran Samivel1,2,*, Dae Woo Kim3,6,*, Hye Ran Son1, Yun-Hee Rhee2, Eun Hee Kim1,2, Ji Hye Kim1,2, Jun-Sang Bae2,4, Young-Jun Chung1,2, Phil-Sang Chung1,2, Eyal Raz5 and Ji-Hun Mo1,2,6
1 Department of Otorhinolaryngology, Dankook University College of Medicine, Cheonan, South Korea
2 Beckman Laser Institute Korea, Dankook University College of Medicine, Cheonan, South Korea
3 Department of Otorhinolaryngology-Head and Neck Surgery, Boramae Medical Center, Seoul National University College of Medicine, Seoul, South Korea
4 Department of Premedical Course, Dankook University College of Medicine, Cheonan, South Korea
5 Department of Medicine, University of California, San Diego, La Jolla, California, USA
6 Clinical Mucosal Immunology Study Group
* These auhtors have contributed equally to this work
Ji-Hun Mo, email:
Keywords: allergic rhinitis, BCTC, CD4 T lymphocyte, OVA, TRPV1, Immunology and Microbiology Section, Immune response, Immunity
Received: July 21, 2015 Accepted: November 21, 2015 Published: December 18, 2015
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-κB, 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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