Elena Shashkova

TL;DR: In this paper, the authors highlight recent data on the interactions between T cells and the skeletal system in the context of postmenopausal osteoporosis and review recent studies on the interventions to ameliorate osteoporeosis.

TL;DR: It is shown for the first time how loss of E2 activates low‐grade inflammation to promote the acute phase of bone catabolic activity in ovariectomized (OVX) mice, providing a new mechanism by which E2 regulates the immune system, and how menopause leads to osteoporosis.

TL;DR: Although RANKL directly stimulates osteoclasts to resorb bone, it also controls the osteoclast' ability to induce regulatory T cells, engaging an important negative feedback loop, which has potential relevance to induction of tolerance and autoimmune diseases.

TL;DR: The results of this study demonstrate a novel link between NF-κB signaling and induction of IFN-γ in TcREG and establish an important role forIFN-β in T cREG-mediated protection from bone loss.

TL;DR: These studies provide a basis for using low-dose RANKL as a potential therapeutic for postmenopausal osteoporosis and indicate that antigens presented to CD8+ T cells by osteoclasts are derived from the bone protein matrix because Cathepsin K degrades collagen in the bone.