Phospholipase Cγ in Toll-like receptor-mediated inflammation and innate immunity.

Citation data:

Advances in biological regulation, ISSN: 2212-4934, Vol: 63, Page: 92-97

Publication Year:
2017
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Repository URL:
http://www.sciencedirect.com/science/article/pii/S221249261630032X
PMID:
27707630
DOI:
10.1016/j.jbior.2016.09.006
Author(s):
Bae, Yoe-Sik; Lee, Ha Young; Jung, Young Su; Lee, Mingyu; Suh, Pann-Ghill
Publisher(s):
Elsevier BV
Tags:
Biochemistry, Genetics and Molecular Biology
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review description
Among the phospholipase C (PLC) isoforms, PLCγ not only has unique structural characteristics in terms of harboring SH2 and SH3 domains but also mediates growth factor-induced signaling pathways. PLCγ isoforms are expressed in several innate immune cell types, including macrophages, natural killer cells, mast cells, and neutrophils. Stimulation of Fc receptor or integrin in innate immune cells induces PLCγ activation, which leads to phosphoinositide hydrolysis and calcium increase. The products of PLCγ activity mediate the innate immune response by regulating respiratory burst, phagocytosis, cell adhesion, and cell migration. PLCγ also regulates the inflammatory response by affecting Toll-like receptor-mediated signaling. Here, we briefly review the current understanding of the functional role of PLCγ in inflammation and innate immunity in some innate immune cell types.