Neutrophil: Regulation of Functional Activation and Survival
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".
Deadline for manuscript submissions: closed (31 January 2018) | Viewed by 4432
Special Issue Editor
Interests: regulation of neutrophil functions; survival/apoptosis; inflamamtory cytokines; signal transduction; superoxide production; cytokine production; Toll-like receptors; migration; calpain
Special Issue Information
Dear Colleagues,
Neutrophils play a critical role, not only in the host-defense against invading microorganisms, but also in the tissue injury associated with inflammatory disorders. Neutrophils are rapidly activated by various inflammatory mediators, which include chemotactic factors, chemokines, inflammatory cytokines (such as granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, interferons, and tumor necrosis factor-a) and Toll-like receptor agonists. Neutrophil survival and apoptosis are also affected by these mediators. Activation of neutrophil functions (such as migration, phagocytosis, and superoxide and cytokine production) and neutrophil survival/apoptosis induced by inflammatory mediators are closely associated with the outcome of inflammatory disorders. Recent studies have improved our understanding about the regulatory mechanisms of neutrophil functions and survival/apoptosis at the molecular levels, and further understanding is essential to establish proper treatment of neutrophil-mediated tissue injury. It is expected that this Special Issue may cover recent advances in the regulatory mechanisms of neutrophil functions and survival/apoptosis, which may include the mediator-specific signaling pathways (such as mitogen-activated protein kinases, phosphatidylinositol 3-kinase, and Janus kinases).
Prof. Dr. Seiichi Kitagawa
Guest Editor
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Keywords
- neutrophil functions
- inflammatory cytokines
- signaling pathway
- survival/apoptosis
- Toll-like receptors
- migration
- mitogen-activated protein kinases
- chemotactic factors
- calpain
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