期刊
ANNUAL REVIEW OF IMMUNOLOGY VOL 33
卷 33, 期 -, 页码 49-77出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-immunol-032414-112306
关键词
IL-1 beta; caspase-1; inflammasome-independent; serine proteases; host defense
类别
资金
- NATIONAL CANCER INSTITUTE [P30CA046934] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI015614, R37AI015614] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR045584] Funding Source: NIH RePORTER
- NCI NIH HHS [CA-046934] Funding Source: Medline
- NIAID NIH HHS [AI-15614] Funding Source: Medline
- NIAMS NIH HHS [AR-45584] Funding Source: Medline
Induction, production, and release of proinflammatory cytokines are essential steps to establish an effective host defense. Cytokines of the interleukin-1 1 (IL-1) family induce inflammation and regulate T lymphocyte responses while also displaying homeostatic and metabolic activities. With the exception of the IL-1 receptor antagonist, all IL-1 family cytokines lack a signal peptide and require proteolvtic processing into an active molecule. One such unique protease is caspase-1, which is activated by protein platforms called the inflammasomes. However, increasing evidence suggests that inflasomes and caspase-1 are not the only mechanism for processing IL-1 cytokines. IL-1 cytokines are often released as precursors and require extracellular processing for activity. Here we review the inflammasome-independent enzymatic processes that are able to activate IL-1 cytokines, paying special attention to neutrophil-derived serine proteases, which subsequently induce inflammation and modulate host defense. The inflammasome-independent processing of IL-1 cytokines has important consequences for understanding inflammatory diseases, and it impacts the design of IL-1-based modulatory therapies.
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