Abstract
During evolution, the bony skeleton and the adaptive immune system have coevolved in vertebrate animals. The shared evolutionary origin and bone marrow microenvironments apparently provided the two systems with common molecules involved in individual cell lineage differentiation and function. In fact, the bone and immune systems share abundant molecules and regulatory mechanisms in the maintenance of physiologic function. Furthermore, dysregulated interactions between the immune and skeletal systems frequently result in pathological conditions affecting both systems. In humans, the most frequent skeletal pathologies are associated with bone loss through the excessive activity of osteoclasts. T cells represent the major regulatory players in bone destruction in inflammation. In this review we focus on the shared mechanisms and interactions between osteoclasts and T cells. Understanding these apparently different cell lineages in an integrated functional context should provide a molecular basis for developing novel therapeutic approaches to bone and inflammatory diseases.
