IL-33 is expressed in human osteoblasts, but has no direct effect on bone remodeling

Saïdi, Soraya; Bouri, F.; Lencel, P.; Duplomb, Laurence; Baud’huin, Marc; Delplace, Séverine; Leterme, Damien; Miellot, Flore; Heymann, Dominique; Hardouin, Pierre; Palmer, Gaby; Magne, David

doi:10.1016/j.cyto.2010.11.021

Cited by 53 publications

(46 citation statements)

References 50 publications

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“…This phenomenon may also explain the lack of an inhibitory effect of IL-33 on osteoclast development from human peripheral blood CD14 + cells as observed by us and by others (35,36). This finding is in agreement with an increasing number of studies suggesting the existence of various subsets of human and murine circulating monocytes that differ in their cytokine profile, migratory properties, surface markers, and function.…”

Section: Discussionsupporting

confidence: 80%

IL-33 Shifts the Balance from Osteoclast to Alternatively Activated Macrophage Differentiation and Protects from TNF-α–Mediated Bone Loss

Zaiss

Kurowska‐Stolarska

Böhm

et al. 2011

The Journal of Immunology

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IL-33 is a new member of the IL-1 family, which plays a crucial role in inflammatory response, enhancing the differentiation of dendritic cells and alternatively activated macrophages (AAM). Based on the evidence of IL-33 expression in bone, we hypothesized that IL-33 may shift the balance from osteoclast to AAM differentiation and protect from inflammatory bone loss. Using transgenic mice overexpressing human TNF, which develop spontaneous joint inflammation and cartilage destruction, we show that administration of IL-33 or an IL-33R (ST2L) agonistic Ab inhibited cartilage destruction, systemic bone loss, and osteoclast differentiation. Reconstitution of irradiated hTNFtg mice with ST2−/− bone marrow led to more bone loss compared with the chimeras with ST2+/+ bone marrow, demonstrating an important endogenous role of the IL-33/ST2L pathway in bone turnover. The protective effect of IL-33 on bone was accompanied by a significant increase of antiosteoclastogenic cytokines (GM-CSF, IL-4, and IFN-γ) in the serum. In vitro IL-33 directly inhibits mouse and human M-CSF/receptor activator for NF-κB ligand-driven osteoclast differentiation. IL-33 acts directly on murine osteoclast precursors, shifting their differentiation toward CD206+ AAMs via GM-CSF in an autocrine fashion. Thus, we show in this study that IL-33 is an important bone-protecting cytokine and may be of therapeutic benefit in treating bone resorption.

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Section: Discussionsupporting

confidence: 80%

IL-33 Shifts the Balance from Osteoclast to Alternatively Activated Macrophage Differentiation and Protects from TNF-α–Mediated Bone Loss

Zaiss

Kurowska‐Stolarska

Böhm

et al. 2011

The Journal of Immunology

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“…While our findings contribute to the understanding of how IL-33 affects Th2-mediated diseases, it is not clear how IL-33 may function in these Th17-mediated diseases. IL-33 has been shown to cause a wide range of effects, including neutrophil migration, mast cell activation, osteoclast and osteoblast function, wound healing, and others (69)(70)(71). Thus, the ability of IL-33 to affect disease pathogenesis through a multitude of mechanisms has made it an intriguing area of investigation in which a great deal still remains unknown.…”

Section: Discussionmentioning

confidence: 99%

IL-33–dependent induction of allergic lung inflammation by FcγRIII signaling

Tjota¹,

Williams²,

Lu³

et al. 2013

J. Clin. Invest.

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Atopic asthma is a chronic inflammatory disease of the lungs generally marked by excessive Th2 inflammation. The role of allergen-specific IgG in asthma is still controversial; however, a receptor of IgG-immune complexes (IgG-ICs), FcγRIII, has been shown to promote Th2 responses through an unknown mechanism. Herein, we demonstrate that allergen-specific IgG-ICs, formed upon reexposure to allergen, promoted Th2 responses in two different models of IC-mediated inflammation that were independent of a preformed T cell memory response. Development of Th2-type airway inflammation was shown to be both FcγRIII and TLR4 dependent, and T cells were necessary and sufficient for this process to occur, even in the absence of type 2 innate lymphoid cells. We sought to identify downstream targets of FcγRIII signaling that could contribute to this process and demonstrated that bone marrow-derived DCs, alveolar macrophages, and respiratory DCs significantly upregulated IL-33 when activated through FcγRIII and TLR4. Importantly, IC-induced Th2 inflammation was dependent on the ST2/IL-33 pathway. Our results suggest that allergen-specific IgG can enhance secondary responses by ligating FcγRIII on antigen-presenting cells to augment development of Th2-mediated responses in the lungs via an IL-33-dependent mechanism.

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“…IL-33 is expressed by bone-forming osteoblasts [10]. Moreover, recent studies reported that IL-33 was expressed in bone tissue, where it plays an important role in bone remodeling by effectively blocking osteoclastogenesis [10,11]; however, the mechanisms underlying the effects of IL-33 on osteoclast formation and function are largely unknown.…”

Section: Introductionmentioning

confidence: 99%

IL-33 inhibits RANKL-induced osteoclast formation through the regulation of Blimp-1 and IRF-8 expression

Kiyomiya

Ariyoshi

Okinaga

et al. 2015

Biochemical and Biophysical Research Communications

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IL-33 is expressed in human osteoblasts, but has no direct effect on bone remodeling

Cited by 53 publications

References 50 publications

IL-33 Shifts the Balance from Osteoclast to Alternatively Activated Macrophage Differentiation and Protects from TNF-α–Mediated Bone Loss

IL-33 Shifts the Balance from Osteoclast to Alternatively Activated Macrophage Differentiation and Protects from TNF-α–Mediated Bone Loss

IL-33–dependent induction of allergic lung inflammation by FcγRIII signaling

IL-33 inhibits RANKL-induced osteoclast formation through the regulation of Blimp-1 and IRF-8 expression

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