H. Takayanagi

Publications330
h-index78
Citations29,357
Highly Influential Citations1,542
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Induction and activation of the transcription factor NFATc1 (NFAT2) integrate RANKL signaling in terminal differentiation of osteoclasts.
Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems
TLDR
The two systems should be understood to be integrated and operating in the context of the 'osteoimmune' system, a heuristic concept that provides not only a framework for obtaining new insights by basic research, but also a scientific basis for the discovery of novel treatments for diseases related to both systems.
The molecular understanding of osteoclast differentiation.
Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis
TLDR
It is shown that mice lacking immunoreceptor tyrosine-based activation motif (ITAM)-harbouring adaptors, Fc receptor common γ subunit (FcRγ) and DNAX-activating protein (DAP)12, exhibit severe osteopetrosis owing to impaired osteoclast differentiation.
Evidence for osteocyte regulation of bone homeostasis through RANKL expression
TLDR
It is found that purified osteocytes express a much higher amount of receptor activator of nuclear factor-κB ligand (RANKL) and have a greater capacity to support osteoclastogenesis in vitro than osteoblasts and bone marrow stromal cells.
RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-β
TLDR
This study shows that RANKL induces the interferon-β (IFN- β) gene in osteoclast precursor cells, and that IFN-β inhibits the differentiation by interfering with the RankL-induced expression of c-Fos, an essential transcription factor for the formation of osteoclasts.
Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction
TLDR
Th17 is a powerful therapeutic target for the bone destruction associated with T cell activation and the interleukin (IL)-23–IL-17 axis, rather than the IL-12–IFN-γ axis, is critical for the onset phase of autoimmune arthritis.
Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis
TLDR
It is shown that TH17 cells originating from Foxp3+ T cells have a key role in the pathogenesis of autoimmune arthritis.
Autoamplification of NFATc1 expression determines its essential role in bone homeostasis
TLDR
It is established that NFATc1 represents a potential therapeutic target for bone disease and a mechanism that underlies the essential role of NF ATc1 in bone homeostasis is revealed.
T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-gamma.
TLDR
This study shows that there is cross-talk between the tumour necrosis factor and IFN families of cytokines, through which IFN-gamma provides a negative link between T-cell activation and bone resorption and may offer a therapeutic approach to treat the inflammation-induced tissue breakdown.
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