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Published on: November 6, 2014
Immune regulation of bone loss by Th17 cells in oestrogen-deficient osteoporosis
1College of Physical Education and Health Sciences, Zhejiang Normal University, Jinhua, Zhejiang, China.
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.
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