[Role of the immune system in the pathophysiology of postmenopausal osteoporosis].

The immune system plays a critical role in the pathophysiology of postmenopausal osteoporosis. Estrogen deficiency induces mild increase in production of proinflammatory cytokines, such as IL-1, IL-6, and TNF-alpha, systemically and locally, which promotes osteoclastogenesis in the bone marrow. The most important cytokine in the context of estrogen deficiency-induced bone loss has been shown to be TNF-alpha produced by bone marrow T-lymphocytes that are stimulated through a complex mechanism involving antigen-presenting cells and various cytokines including IL-7, IFN-gamma, and TGF-beta. Proinflammatory cytokines also suppress osteoblastogenesis, while the crosstalk between T-lymphocytes and marrow stromal cells regulates the osteoclastogenic activity of the latter. Counteracting these interactions could be a novel strategy for osteoporosis treatment.