Anti-Human RANKL Recombinant Antibody Fab Fragment (CAT#: TAB-310CT-F(E))

Zhao, Wenbin, et al. "Synovial fibroblasts regulate the cytotoxicity and osteoclastogenic activity of synovial natural killer cells through the RANKL-RANK axis in osteoarthritis." Scandinavian Journal of Immunology 94.2 (2021): e13069. https://doi.org/10.1111/sji.13069

This study investigates the role of the RANKL-RANK axis in modulating natural killer (NK) cell function in osteoarthritis (OA). Using a rat collagenase-induced OA model, the researchers found that compared to splenic NK cells, synovial NK cells showed reduced cytotoxicity and lower production of IFN-γ, perforin, and granzyme B when stimulated with IL-12, IL-15, and IL-18. The study reveals that synovial NK cells highly express RANK (receptor activator of nuclear factor-κB), while OA synovial fibroblasts (SFs) upregulate RANKL (RANK ligand) expression. Through co-culture experiments, the researchers demonstrated that OA SFs inhibit NK cell cytotoxicity but promote their osteoclastogenic activity through the RANKL-RANK signaling pathway.
Creative Biolabs provided a RANKL neutralizing antibody (CAT# TAB-310CT-F(E)) that was crucial for demonstrating the involvement of RANKL in NK cell-mediated osteoclast formation. When this antibody was added to the NK cell-bone marrow cell co-cultures, it significantly suppressed osteoclast generation, confirming that RANKL plays a central role in the osteoclastogenic effect of NK cells. This finding helped establish a novel mechanism by which synovial fibroblasts modulate NK cell reactivity in OA, potentially opening new avenues for therapeutic interventions targeting the RANKL-RANK axis to address bone loss in osteoarthritis.