Regulation of immune system affecting bone turnover

The regulation of immune system affecting bone turnover refers to the complex, bidirectional interaction between immune cells and bone cells—fields collectively studied under osteoimmunology. Immune cells, including T cells (Th1, Th17, Treg), B cells, macrophages, and their secreted cytokines (e.g., RANKL, IFN-γ, TNF-α, IL-17, OPG), play crucial roles in regulating bone resorption (via osteoclasts) and formation (via osteoblasts)[1][2][3][4][5][6]. Under normal conditions, this interplay maintains bone homeostasis, but in chronic inflammation or immune dysregulation (such as in rheumatoid arthritis or osteoporosis), heightened immune activation leads to increased osteoclastogenesis, bone resorption, and net bone loss. Therapeutic interventions increasingly target these immune–bone interactions to prevent or treat bone diseases associated with immune dysfunction[1][4][5]. This query does not represent a canonical molecular drug target but rather a biological process or pathway involving numerous cellular and molecular actors. For structured data extraction or ontology work, this entry should be flagged or curated as a process or pathway, not as a classical target[1][2][3][4][5][6].

Other names

osteoimmunologyimmune regulation of bone turnoverimmune–bone axis

Immune modulators work by altering immune cell activity or cytokine signaling, e.g., TNF-α blockade reduces inflammation-induced bone loss.