학술논문

Pathogenic helper T cells as the novel therapeutic targets for immune-mediated intractable diseases.
Document Type
Academic Journal
Author
Onodera A; Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan; Institute for Advanced Academic Research, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.; Kokubo K; Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.; Okano M; Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.; Onoue M; Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.; Kiuchi M; Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.; Iwamura C; Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.; Iinuma T; Department of Otorhinolaryngology, Head and Neck Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.; Kimura MY; Department of Experimental Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan; Chiba University 'Synergy Institute for Futuristic Mucosal Vaccine Research and Development (cSIMVa), Japan Initiative for World-leading Vaccine Research and Development Centers, Japan Agency for Medical Research and Development (AMED), Chiba, Japan.; Ebihara N; Department of Ophthalmology, Juntendo University Urayasu Hospital, Chiba 279-0021, Japan.; Hanazawa T; Department of Otorhinolaryngology, Head and Neck Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.; Nakayama T; Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan; AMED-CREST, AMED, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan. Electronic address: tnakayama@faculty.chiba-u.jp.; Hirahara K; Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan; Chiba University 'Synergy Institute for Futuristic Mucosal Vaccine Research and Development (cSIMVa), Japan Initiative for World-leading Vaccine Research and Development Centers, Japan Agency for Medical Research and Development (AMED), Chiba, Japan. Electronic address: hiraharak@chiba-u.jp.
Source
Publisher: Pergamon Press Country of Publication: England NLM ID: 7905840 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-016X (Electronic) Linking ISSN: 01637258 NLM ISO Abbreviation: Pharmacol Ther Subsets: MEDLINE
Subject
Language
English
Abstract
Allergic diseases arise from a complex interplay between immune system and environmental factors. A link between the pathogenesis of allergic diseases and type 2 immune responses has become evident, with conventional and pathogenic type 2 helper T (Th2) cells involved in both. Recently, there has been a significant development in therapeutic agents for allergic diseases: IL-5 and IL-5 receptor antagonists, Janus kinase (JAK) inhibitors, and sublingual immunotherapy (SLIT). Mepolizumab, an IL-5, and Benralizumab, an IL-5 receptor antagonist, modulate eosinophilic inflammation mediated by IL-5-producing Th2 cells. Delgocitinib shows that JAK-associated signaling is essential for the inflammatory reaction in atopic dermatitis, one of the common allergic diseases. SLIT has a significant effect on allergic rhinitis by reducing pathogenic Th2 cell numbers. More recently, novel molecules that are involved in pathogenic Th2 cell-mediated allergic diseases have been identified. These include calcitonin gene-related peptide (CGRP), reactive oxygen species (ROS) scavenging machinery regulated by the Txnip-Nrf2-Blvrb axis, and myosin light chain 9 (Myl9), which interacts with CD69. This review provides an updated view of the recent research on treatment of allergic diseases and their cause: conventional and pathogenic Th2 cells.
Competing Interests: Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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