RANK-L and RANK: T cells, bone loss, and mammalian evolution.

By L. Theill, W. J. Boyle, Josef M. Penninger. Annual Review of Immunology, 2002

843 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/1f91f54235c15b562c1fbb09436e19aa0da433e7

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Citations in the corpus

Denosumab and bisphosphonates: different mechanisms of action and effects. (2011, background): “Considering the role of RANK/RANKL in the ontogenesis of the immune system [21,90] and the widespread expression of these molecules during immune and inflammatory reactions, where they appear to play a role as co-stimulatory factors for the activation of T cells and dendritic cells [9], one would ex”
Osteoimmunology: interplay between the immune system and bone metabolism. (2006, background): “Initial studies of TRANCE- and RANK-deficient mice demonstrated the importance of these signals for secondary lymphoid organ development, as these animals display a lack of peripheral lymph nodes and abnormalities in B cell follicle formation and marginal zone integrity in the spleen (58, 59).”
Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction (2006, background): “been shown to be expressed by T cells, indicating that RANKL is a molecule that bridges the skeletal and immune systems (4).”
Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems (2007, background): “and receptor activator of nuclear factor-κB ( NF-κB ) ligand ( RANKL ; also known as TNFSF11), a tumour-necrosis factor (TNF)-family cytokin”
Osteoclast differentiation and activation (2003, background): “Hormones and factors that stimulate bone resorption in vivo induce the expression of RANKL on osteogenic stromal cell”
Inflammatory and immune pathways in the pathogenesis of periodontal disease (2014, background): “It is now clear that RANKL and osteoprotegerin are the key regulators of bone remodeling and are directly in- volved in the differentiation, activation and survival of osteoclasts and osteoclast precursors (2, 129, 261).”
NF-κB in biology and targeted therapy: new insights and translational implications (2024, background): “96 RANK-activated non-canonical NF-κ B signaling promotes osteoclasto-genesis and differentiation.”
Receptor activator of nuclear factor kappaB ligand and osteoprotegerin regulation of bone remodeling in health and disease. (2008, neutral): “Those findings led investigators to consider that these developmental processes were linked (168).”