PLCγ2: Where bone and immune cells find their common ground

Roberta Faccio, Viviana Cremasco

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

21 Scopus citations


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.

Original languageEnglish
Title of host publicationSkeletal Biology and Medicine
PublisherBlackwell Publishing Inc.
Number of pages7
ISBN (Print)9781573317856
StatePublished - Mar 2010

Publication series

NameAnnals of the New York Academy of Sciences
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632


  • Arthritis
  • Bone
  • Inflammation
  • Neutrophils
  • Osteoclasts
  • PLCγ2


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