Bone cells and immune cells share the same microenvironments in the bone marrow, communicating through various factors. Osteoblasts, osteoclasts and osteocytes are not only degrading or forming bone but may have distinct roles in the immune regulation. The interdisciplinary filed, osteoimmunology, studying the interaction and shared molecules between bone and immune systems is important for many fields including medical researches such as rheumatology and dental researches in addition to basic researches on bone and immune systems. Here I summarize the recent advance in the field of osteoimmunology and its relevance in the sepsis-induced immunodeficiency mediated by loss of osteoblasts.

Sepsis is a host inflammatory response to severe infection associated with high mortality that is partly caused by lymphopenia-associated immunodeficiency. We found that sepsis rapidly ablated osteoblasts and induced the reduction of the common lymphoid progenitor (CLP) number, leading to the severe lymphopenia. Osteoblast ablation or inducible deletion of interleukin-7 (IL-7) in osteoblasts recapitulated the lymphopenic phenotype and a lower CLP number without affecting hematopoietic stem cells (HSCs). Pharmacological activation of osteoblasts through PTH administration improved sepsis-induced lymphopenia. This study features a reciprocal interaction between the immune and bone systems, in which acute inflammation induces a defect in bone cells resulting in immunodeficiency.