Interleukin 7 and estrogen-induced bone loss.
During the past decade, we have increased greatly our understanding of the pathogenesis of postmenopausal osteoporosis, a major cause of morbidity and mortality. We know now that estrogen regulates the expression of cytokines that target cell types involved in modulating bone turnover. Although early work demonstrated that tumor necrosis factor alpha plays an important role in regulating bone mass, recent studies also implicate the lymphopoietic molecule interleukin 7. This protein is unique in that it suppresses the bone-forming osteoblast, whilst stimulating formation and function of the osteoclast, the exclusive resorptive cell. Furthermore, the latest findings confirm and expand the concept that T cells are key mediators of bone loss following gonadal failure.
Ross
F Patrick
FP
Department of Pathology and Immunology, Washington University School of Medicine, Barnes-Jewish Hospital, MS 90-31-649, 216 S. Kingshighway, St Louis, MO 63110, USA. rossf@medicine.wustl.edu
D000818:Animals; D001842:Bone and Bones / Q000378:metabolism; D002454:Cell Differentiation; D016207:Cytokines / Q000378:metabolism; D004967:Estrogens / Q000378:metabolism*; D006801:Humans; D015851:Interleukin-7 / Q000378:metabolism*; D010006:Osteoblasts / Q000378:metabolism; D010010:Osteoclasts / Q000378:metabolism; D010024:Osteoporosis / Q000276:immunology / Q000378:metabolism*; D015663:Osteoporosis, Postmenopausal / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D004967:Estrogens; D015851:Interleukin-7; D014409:Tumor Necrosis Factor-alpha