期刊
INTERNATIONAL IMMUNOLOGY
卷 31, 期 9, 页码 607-615出版社
OXFORD UNIV PRESS
DOI: 10.1093/intimm/dxz044
关键词
BLT1; CysLT1; CysLT2; GPR99
类别
资金
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of the Japan Society for the Promotion of Science (JSPS) [22116001, 22116002, 15H05897, 15H05904, 15H04708, 18H02627]
- Naito Foundation
- Ono Medical Research Foundation
- Uehara Memorial Foundation
- Mitsubishi Foundation
- Takeda Science Foundation
- Foundation for Strategic Research Projects in Private Universities of the MEXT [S1311011]
- Institute for Environmental and Gender-Specific Medicine
- Grants-in-Aid for Scientific Research [18H02627, 22116001, 15H04708, 15H05904, 22116002] Funding Source: KAKEN
Leukotrienes (LTs) are inflammatory mediators derived from arachidonic acid. LTs include the di-hydroxy acid LT (LTB 4) and the cysteinyl LTs (CysLTs; LTC4, LTD4 and LTE4), all of which are involved in both acute and chronic inflammation. We and other groups identified a high-affinity LTB4 receptor, BLT1; the LTC4 and LTD4 receptors, CysLT1 and CysLT2; and the LTE4 receptor, GPR99. Pharmacological studies have shown that BLT1 signaling stimulates degranulation, chemotaxis and phagocytosis of neutrophils, whereas CysLT1 and CysLT2 signaling induces airway inflammation by increasing vascular permeability and the contraction of bronchial smooth muscle. Recently, we and other groups suggested that the LTB 4-BLT1 axis and the cysteinyl LTs-CysLT1/2 axis are involved in chronic inflammatory diseases including asthma, atopic dermatitis, psoriasis, atherosclerosis, arthritis, obesity, cancer and age-related macular degeneration using animal models for disease and gene knockout mice. This review describes the classical and novel functions of LTs and their receptors in several inflammatory diseases and discusses the potential clinical applications of antagonists for LT receptors and inhibitors of LT biosynthesis.
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