期刊
NATURE IMMUNOLOGY
卷 20, 期 9, 页码 1138-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41590-019-0467-1
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资金
- University of Colorado Cancer Center NIH at the University of Colorado Anschutz Medical Campus [P30CA046934]
- Oticon Foundation
- Lundbeck Foundation
- Knud Hojgaard Foundation
- Interleukin Foundation
- NIH [HL126736, ES025534, HL135872-01, AI-15614]
Interleukin (IL)-1R3 is the co-receptor in three signaling pathways that involve six cytokines of the IL-1 family (IL-1 alpha, IL-1 beta, IL-33, IL-36 alpha, IL-36 beta and IL-36 gamma). In many diseases, multiple cytokines contribute to disease pathogenesis. For example, in asthma, both IL-33 and IL-1 are of major importance, as are IL-36 and IL-1 in psoriasis. We developed a blocking monoclonal antibody (mAb) to human IL-1R3 (MAB-hR3) and demonstrate here that this antibody specifically inhibits signaling via IL-1, IL-33 and IL-36 in vitro. Also, in three distinct in vivo models of disease (crystal-induced peritonitis, allergic airway inflammation and psoriasis), we found that targeting IL-1R3 with a single mAb to mouse IL-1R3 (MAB-mR3) significantly attenuated heterogeneous cytokine-driven inflammation and disease severity. We conclude that in diseases driven by multiple cytokines, a single antagonistic agent such as a mAb to IL-1R3 is a therapeutic option with considerable translational benefit.
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