The role of TRPV1 in the CD4 + T cell-mediated inflammatory response of allergic rhinitis

// Ramachandran Samivel 1,2,* , Dae Woo Kim 3,6,* , Hye Ran Son 1 , Yun-Hee Rhee 2 , Eun Hee Kim 1,2 , Ji Hye Kim 1,2 , Jun-Sang Bae 2,4 , Young-Jun Chung 1,2 , Phil-Sang Chung 1,2 , Eyal Raz 5 and Ji-Hun Mo 1,2,6 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 PremedicalCourse, Dankook University College of Medicine, Cheonan, South Korea 5 Department of Medicine, University of California, San Diego, La Jolla, California, USA 6 Clinical Mucosal ImmunologyStudy Group * These auhtors have contributed equally to this work Correspondence to: 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 Abstract Transient receptor potential vanilloid1 ( 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 TRPV1in CD4 + T cell in allergic rhinitis remains poorly understood. In this study, TRPV1expression was localized in CD4 + T cells. Both knockout and chemical inhibition of TRPV1suppressed 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 TRPV1knockout 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 TRPV1antagonists, 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, TRPV1activation on CD4 + T cells is involved in T cell receptor signaling, and it could be a novel therapeutic target in AR.