title: Phospholipase Cγ in Toll-like receptor-mediated inflammation and innate immunity.
abstract: 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.
authors.affiliation: Department of Biological Sciences, Sungkyunkwan University, Suwon 16419, Republic of Korea; Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Republic of Korea. Electronic address: yoesik@skku.edu.
authors.forename: Yoe-Sik
authors.initials: YS
authors.lastname: Bae
authors.affiliation: Department of Biological Sciences, Sungkyunkwan University, Suwon 16419, Republic of Korea.
authors.forename: Ha Young
authors.initials: HY
authors.lastname: Lee
authors.affiliation: Department of Biological Sciences, Sungkyunkwan University, Suwon 16419, Republic of Korea.
authors.forename: Young Su
authors.initials: YS
authors.lastname: Jung
authors.affiliation: Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul 06351, Republic of Korea.
authors.forename: Mingyu
authors.initials: M
authors.lastname: Lee
authors.affiliation: School of Nano-Biotechnology and Chemical Engineering, Ulsan National Institute of Science and Technology, Ulsan 44919, Republic of Korea.
authors.forename: Pann-Ghill
authors.initials: PG
authors.lastname: Suh
mesh_terms: D000818:Animals; D002465:Cell Movement / Q000276:immunology; D005786:Gene Expression Regulation; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000201:enzymology* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D007694:Killer Cells, Natural / Q000201:enzymology* / Q000276:immunology; D008264:Macrophages / Q000201:enzymology* / Q000276:immunology; D008407:Mast Cells / Q000201:enzymology* / Q000276:immunology; D009504:Neutrophils / Q000201:enzymology* / Q000276:immunology; D010587:Phagocytosis / Q000235:genetics; D051966:Phospholipase C gamma / Q000737:chemistry / Q000235:genetics / Q000276:immunology*; D000072417:Protein Domains; D011961:Receptors, Fc / Q000235:genetics / Q000276:immunology; D016897:Respiratory Burst / Q000276:immunology; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000235:genetics / Q000276:immunology
chemical_list: D011961:Receptors, Fc; D051193:Toll-Like Receptors; D051966:Phospholipase C gamma