Exophilin-5 Regulates Allergic Airway Inflammation by Controlling IL-33–Mediated Th2 Responses
The Journal of Clinical Investigation RESEARCH ARTICLE Exophilin-5 regulates allergic airway inflammation by controlling IL-33–mediated Th2 responses Katsuhide Okunishi,1 Hao Wang,1 Maho Suzukawa,2,3 Ray Ishizaki,1 Eri Kobayashi,1 Miho Kihara,4 Takaya Abe,4,5 Jun-ichi Miyazaki,6 Masafumi Horie,7 Akira Saito,7 Hirohisa Saito,8 Susumu Nakae,9 and Tetsuro Izumi1 1Laboratory of Molecular Endocrinology and Metabolism, Department of Molecular Medicine, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan. 2National Hospital Organization Tokyo National Hospital, Tokyo, Japan. 3Division of Respiratory Medicine and Allergology, Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan. 4Laboratory for Animal Resource Development and 5Genetic Engineering, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan. 6Institute of Scientific and Industrial Research, Osaka University, Osaka, Japan. 7Department of Respiratory Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. 8Department of Allergy and Clinical Immunology, National Research Institute for Child Health and Development, Tokyo, Japan. 9Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. A common variant in the RAB27A gene in adults was recently found to be associated with the fractional exhaled nitric oxide level, a marker of eosinophilic airway inflammation. The small GTPase Rab27 is known to regulate intracellular vesicle traffic, although its role in allergic responses is unclear. We demonstrated that exophilin-5, a Rab27-binding protein, was predominantly expressed in both of the major IL-33 producers, lung epithelial cells, and the specialized IL-5 and IL-13 producers in the CD44hiCD62LloCXCR3lo pathogenic Th2 cell population in mice.
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