Unmet Need:
According to the NIH, up to 24 million Americans suffer from autoimmune disease and the prevalence is rising. Additionally, by 2020 one in two Americans over age 50 are expected to be at risk for developing osteoporosis of the hip and even more will be at risk developing osteoporosis at any site in the skeleton. Research is ongoing to hinder bone loss as well as automimmune diseases such as rheumatoid arthritis. There have been therapies developed inhibiting the interaction between receptor activator of the NF-kappaB ligand (RANKL)/receptor activator of the NF-kappaB (RANK) which is a crucial step to forming mature osteoclasts, cells that play a role in bone resorption. More mature osteoclast formation can leads to higher degree of bone loss. There is a good understanding of the underlying mechanisms of these diseases, however there is a lack of knowledge of the mechanism of fusion of preosteoclasts to form mature osteoclasts.
Technology Overview:
The current technology reports mechanistic insight into the osteoclast fusion process via the important interaction of Siglec-15 and TLR2, which are cell surface proteins whose interaction initiates fusion of preosteoclasts differentiating self from non-self. Furthermore, they have found that Siglec15 expression is activated by M-CSF while TLR2 sialylation is induced by RANKL, indicating that both M-CSF and RANKL are required for the formation of the recognition signal for osteoclast fusion.
Stage of Development:
Technology is ready for licensing.
Publications:
Manuscript in preparation.
