Premium
PLCγ2: where bone and immune cells find their common ground
Author(s) -
Faccio Roberta,
Cremasco Viviana
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.05217.x
Subject(s) - rankl , immune system , osteoimmunology , osteoclast , inflammation , microbiology and biotechnology , immunology , integrin , signal transduction , chemistry , arthritis , regulator , receptor , medicine , biology , activator (genetics) , biochemistry , gene
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.