Journal
IMMUNOLOGICAL REVIEWS
Volume 273, Issue 1, Pages 121-139Publisher
WILEY
DOI: 10.1111/imr.12455
Keywords
neutrophils; Fc-receptors; integrins; protein kinases/phosphatases; inflammation; signal transduction
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Funding
- Lendulet program of the Hungarian Academy of Sciences [LP2013-66/2013]
- Wellcome Trust International Senior Research Fellowship [087782]
- Hungarian National Excellence Program - EU's European Social Fund [TAMOP 4.2.4. A/1-11-1-2012-0001]
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Neutrophils play a critical role in antimicrobial host defense, but their improper activation also contributes to inflammation-induced tissue damage. Therefore, understanding neutrophil biology is important for the understanding, diagnosis, and therapy of both infectious and inflammatory diseases. Neutrophils express a large number of cell-surface receptors that sense extracellular cues and trigger various functional responses through complex intracellular signaling pathways. During the last several years, we and others have shown that tyrosine kinases play a critical role in those processes. In particular, Src-family and Syk tyrosine kinases couple Fc-receptors and adhesion receptors (integrins and selectins) to various neutrophil effector functions. This pathway shows surprising similarity to lymphocyte antigen receptor signaling and involves various other enzymes (e.g. PLC gamma 2), exchange factors (e.g. Vav-family members) and adapter proteins (such as ITAM-containing adapters, SLP-76, and CARD9). Those mediators trigger various antimicrobial functions and play a critical role in coordinating the inflammatory response through the release of inflammatory mediators, such as chemokines and LTB4. Interestingly, however, tyrosine kinases have a limited direct role in the migration of neutrophils to the site of inflammation. Here, we review the role of tyrosine kinase signaling pathways in neutrophils and how those pathways contribute to neutrophil activation in health and disease.
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