Immune regulation of bone loss by Th17 cells in oestrogen-deficient osteoporosis.

BACKGROUND

The role of T helper (Th) 17 cells in autoimmune diseases has been extensively studied recently, but its function in oestrogen-deficient osteoporosis remains undefined. This review aimed to explore the role of Th17 cells in regulating bone loss induced by oestrogen deficiency.

MATERIALS AND

METHODS

We searched PubMed, Embase, Google Scholar and Biosis up to 1 February 2013 for immune regulation of oestrogen-deficient osteoporosis by Th17 cells. Terms relevant to immunity, oestrogen deficiency, osteoporosis and Th17 cells were used for database searching. Seventy-five papers met the predetermined searching criteria.

RESULTS

Studies indicate Th17 lineage to be a potent osteoclastogenic mediator in oestrogen-deficient osteoporosis. Oestrogen deficiency promotes osteoclastogenesis by up-regulating Th17 cell populations in bone marrow and IL-17 levels in peripheral blood. Meanwhile, transcription factors involved in Th17 cell differentiation, such as RORγt and RORα, are highly expressed in ovariectomized animals. Treatment with IL-17 significantly promotes production of RANKL, TNF and IL-6 as well as TRAP(+) cells in culture; blocking IL-17 pathway significantly reduces abundance of Th17 cells and effectively prevents bone loss in ovariectomized mice.

CONCLUSIONS

The main body of literatures suggests Th17 to be a critical modulator in the pathogenesis of oestrogen-deficient osteoporosis, which supports the notion that oestrogen-deficient osteoporosis is a complex interplay between oestrogen, osteoclastogenic cytokines and osteoclasts. In addition, therapeutic strategies targeting IL-17 networks may be clinically useful in treatment for postmenopausal osteoporosis.