TRANCE together with IL‐7 induces pre‐B cells to proliferate

Kato, Ibuki; Sato, Hiromu; Kudo, Akira

doi:10.1002/immu.200310007

Cited by 8 publications

(6 citation statements)

References 60 publications

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“…Both osteoclast precursors and B lymphocytes are derived from HSCs. B‐lymphoid lineage cells in early developmental stages express receptor activator of nuclear factor κB (RANK) ligand (RANKL) (55, 56). Both IL‐7‐dependent and IL‐7‐independent pre‐B‐cell lines expressed RANKL (56).…”

Section: Il‐7 and Osteoclastsmentioning

confidence: 99%

“…B‐lymphoid lineage cells in early developmental stages express receptor activator of nuclear factor κB (RANK) ligand (RANKL) (55, 56). Both IL‐7‐dependent and IL‐7‐independent pre‐B‐cell lines expressed RANKL (56). Removal of IL‐7 inhibited RANKL expression from the cultures of IL‐7‐dependent pre‐B cells, and this expression was restored with the addition of IL‐7.…”

Section: Il‐7 and Osteoclastsmentioning

confidence: 99%

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Role of interleukin‐7 in bone and T‐cell homeostasis

Lee

Surh

2005

Immunological Reviews

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Initially defined as a B-cell growth factor, the pleiotropic nature of interleukin-7 (IL-7) has increasingly become appreciated. Besides its well-known roles in B- and T-cell lymphopoiesis, IL-7 is now known to regulate the homeostasis of both mature T cells and bone cells. In bone, the precise nature of how IL-7 affects osteoclasts and osteoblasts is controversial, since it has a variety of actions in different target cells. These activities are gender-specific and are dependent on whether IL-7 is delivered systemically or locally. In mature T cells, IL-7 is essential for the survival of nearly all subsets. Naïve T cells are also dependent on IL-7 for survival and homeostatic proliferation in response to lymphopenia. In addition, IL-7 plays a role in the survival of memory CD8+ cells, and at high concentrations, it can compensate for the absence of IL-15. The role of IL-7 on memory CD4+ cells remains controversial and has yet to be firmly established.

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Section: Il‐7 and Osteoclastsmentioning

confidence: 99%

Section: Il‐7 and Osteoclastsmentioning

confidence: 99%

Role of interleukin‐7 in bone and T‐cell homeostasis

Lee

Surh

2005

Immunological Reviews

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“…Expression of RANKL by tumor cells has been reported in adult T-cell leukemia (24), pre -B-cell leukemia (25), multiple myeloma (26 -28), and prostate cancer (29,30). Furthermore, the expression levels of RANKL on tumor cells have been found to correlate with the severity of lytic bone lesions in multiple myeloma (27,28) and hypercalcemia in adult T-cell leukemia (24), suggesting a causative role for RANKL on tumor cells in the development of lytic bone lesions.…”

Section: Human Cancer Biologymentioning

confidence: 99%

Malignant B-Lymphoid Cells with Bone Lesions Express Receptor Activator of Nuclear Factor-κB Ligand and Vascular Endothelial Growth Factor to Enhance Osteoclastogenesis

Shibata¹,

Abe²,

Hiura³

et al. 2005

Clinical Cancer Research

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Purpose: Receptor activator of nuclear factor-nB ligand (RANKL) is a key mediator of osteoclastogenesis. Because certain types of tumor cells aberrantly express RANKL, and because bone destruction also develops in B-cell lymphomas of bone origin, we investigated RANKL expression and the mechanisms of osteoclastogenesis in B-lymphoid neoplasms. Experimental Design and Results: Immunohistochemistry of bone specimens resected from patients with primary B-cell lymphoma of bone with bone destruction revealed that lymphoma cells express RANKL as well as vascular endothelial cell growth factor (VEGF). The tumor cells isolated from the bone specimens enhanced osteoclastogenesis in vitro. In contrast, B-cell lymphoma infiltrating to the bone marrow without bone destruction did not express RANKL. Both RANKL and VEGF were expressed by a portion of B-lymphoid cell lines, including Daudi and IM-9. These RANKL-expressing tumor cells enhanced osteoclastogenesis from RAW264.7 cells and human monocyte-derived preosteoclasts in the absence of stromal cells/osteoblasts in a RANKL-dependent manner. Furthermore, conditioned media from Daudi cells enhanced transmigration of preosteoclasts that was inhibited by anti-VEGF antibody, suggesting that tumor cell^derived VEGF mediates recruitment of osteoclast precursors. Moreover, cocultures of B-lymphoid cell lines with osteoclasts enhanced the growth of B-lymphoid cells. Conclusions: Some malignant B cells aberrantly express functional RANKL as well as VEGF to enhance osteoclastogenesis. The coexpression of RANKL and VEGF may also contribute to the close cellular interactions with osteoclastic cells, thereby forming a vicious cycle between osteoclastic bone destruction and tumor expansion in bone.Certain types of B-lymphoid neoplasms, such as lymphoma of bone origin and multiple myeloma, exclusively develop and expand in the skeleton. These tumors cause lytic bone lesions, which lead to the debilitating clinical symptoms including intractable bone pain and disabling fractures. In those destructive bone lesions, osteoclasts seem to surround tumor cells and actively resorb bone. Several bone-resorbing factors, including parathyroid hormone -related protein (1), interleukin (IL)-1h (2 -4), and IL-6 (3 -5), have been implicated as causative factors for bone destruction in multiple myeloma, and recent reports including those from ourselves indicate that a C-C chemokine, macrophage inflammatory protein-1a and macrophage inflammatory protein-1h, plays an important role in the development of lytic bone lesions by multiple myeloma (6 -10). However, the pathogenesis as well as the mechanism of bone destruction by B-cell lymphoma of bone origin is largely unknown.Binding of receptor activator of nuclear factor-nB ligand (RANKL; refs. 11 -13) to its receptor (RANK; ref. 14) is essential for the enhancement of osteoclast differentiation, activation, and survival, whereas its decoy receptor, osteoprotegerin (15), inhibits RANKL-RANK signaling. Along with RANKL, macrophage colony-stimulating f...

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“…In addition, IL‐7 production in osteoblasts is required for normal development of B lymphocytes in the bone marrow 22. B‐lymphoid‐lineage cells at early developmental stages express receptor activator of NF‐κB ligand (RANKL)23, 24 in both IL‐7–dependent and IL‐7–independent pre‐B‐cell populations 23. These results indicate that there is an interrelationship between RANKL and IL‐7.…”

Section: Introductionmentioning

confidence: 99%

Osteoblast-specific overexpression of human interleukin-7 rescues the bone mass phenotype of interleukin-7–deficient female mice

Aguila

Mun

Kalinowski

et al. 2012

Journal of Bone and Mineral Research

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Interleukin-7 is a critical cytokine for lymphoid development and a direct inhibitor of in vitro osteoclastogenesis in murine bone marrow cultures. To explore the role of IL-7 in bone, we generated transgenic mouse lines bearing the 2.3 Kb rat collagen 1A1 promoter driving the expression of human IL-7 specifically in osteoblasts. In addition we crossed these mice with IL-7 deficient mice to determine if the alterations in lymphopoiesis, bone mass and osteoclast formation observed in the IL-7 KO mice could be rescued by osteoblast-specific overexpression of IL-7. Here we show that mice overexpressing human IL-7 in the osteoblast lineage demonstrated increased trabecular bone volume in vivo by µCT and decreased osteoclast formation in vitro. Furthermore, targeted overexpression of IL-7 in osteoblasts rescued the osteopenic bone phenotype and B cell development of IL-7 KO mice but did not have an effect on T lymphopoiesis, which occurs in the periphery. The bone phenotypes in IL-7 KO mice and targeted IL-7 overexpressing mouse models were observed only in females. These results likely reflect both a direct inhibitory effects of IL-7 on osteoclastogenesis in vivo and gender specific differences in responses to IL-7.

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TRANCE together with IL‐7 induces pre‐B cells to proliferate

Cited by 8 publications

References 60 publications

Role of interleukin‐7 in bone and T‐cell homeostasis

Role of interleukin‐7 in bone and T‐cell homeostasis

Malignant B-Lymphoid Cells with Bone Lesions Express Receptor Activator of Nuclear Factor-κB Ligand and Vascular Endothelial Growth Factor to Enhance Osteoclastogenesis

Osteoblast-specific overexpression of human interleukin-7 rescues the bone mass phenotype of interleukin-7–deficient female mice

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