@inproceedings{3a80ceb1e74142e58f1083daef4dc6b1,
title = "PLCγ2: Where bone and immune cells find their common ground",
abstract = "Identifying common signaling pathways to bone and immune system may lead to better therapeutic approaches in diseases such as inflammatory arthritis. In this context, PLCγ2 seems to be a promising target. PLCγ2 modulates bone homeostasis by affecting osteoclast recruitment and function. Via its catalytic activity and the adapter domains, PLCγ2 controls RANKL and αvβ3 integrin-dependent signaling pathways in the resorbing cell. Thus, mice lacking PLCγ2 are osteopetrotic. PLCγ2 also regulates neutrophil degranulation after β2 integrin-dependent attachment. Indeed PLCγ2-/- mice are protected from K/BxN serum transfer arthritis, which is known to require neutrophil activation. These studies position PLCγ2 as a critical regulator of the cellular and molecular mechanisms occurring in bone and immune cells during autoimmune inflammation.",
keywords = "Arthritis, Bone, Inflammation, Neutrophils, Osteoclasts, PLCγ2",
author = "Roberta Faccio and Viviana Cremasco",
year = "2010",
month = mar,
doi = "10.1111/j.1749-6632.2009.05217.x",
language = "English",
isbn = "9781573317856",
series = "Annals of the New York Academy of Sciences",
publisher = "Blackwell Publishing Inc.",
pages = "124--130",
booktitle = "Skeletal Biology and Medicine",
}