https://t.co/2yqgY00NjD "PPR-dependent stimulation of TNF production by T cells and the resulting TNF regulation of CD40 signaling in SCs are potential new therapeutic targets for the bone loss of hyperparathyroidism."
https://t.co/2yqgY00NjD "A previously unknown effect of TNF is to increase SC expression of CD40, which in turn increases SC osteoclastogenic activity by upregulating their RANKL/OPG production ratio."
https://t.co/2yqgY00NjD "These findings demonstrate that PPR signaling in T cells plays an essential role in PTH induced bone loss by promoting T cell production of TNF."
https://t.co/2yqgY00NjD "We also show that a novel mechanism by which TNF mediates PTH induced osteoclast formation is upregulation of CD40 expression in SCs, which increases their RANKL/OPG production ratio."
https://t.co/2yqgY00NjD "Recently, it has been reported that T cells are required for cPTH to induce bone loss as the binding of the T cell costimulatory molecule CD40L to SC receptor CD40 augments SC sensitivity to cPTH."
https://t.co/2yqgY00NjD "Hyperparathyroidism in humans and continuous parathyroid hormone (cPTH) treatment in mice cause bone loss by regulating the production of RANKL and OPG by stromal cells (SCs) and osteoblasts (OBs)."
Disruption of PTH Receptor 1 in T Cells Protects against PTH-Induced Bone Loss #CD40 #CD40L #MECFS #LongCovid https://t.co/2yqgY00NjD