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IL-33 shifts the balance from osteoclast to alternatively activated macrophage differentiation and protects from TNF-alpha-mediated bone loss

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IL-33 shifts the balance from osteoclast to alternatively activated macrophage differentiation and protects from TNF-alpha-mediated bone loss. / Zaiss, Mario M; Kurowska-Stolarska, Mariola; Böhm, Christina; Gary, Regina; Scholtysek, Carina; Stolarski, Bartosz; Reilly, James; Kerr, Shauna; Millar, Neal L; Kamradt, Thomas; McInnes, Iain B; Fallon, Padraic G; David, Jean-Pierre; Liew, Foo Y; Schett, Georg.

In: J IMMUNOL, Vol. 186, No. 11, 01.06.2011, p. 6097-105.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Zaiss, MM, Kurowska-Stolarska, M, Böhm, C, Gary, R, Scholtysek, C, Stolarski, B, Reilly, J, Kerr, S, Millar, NL, Kamradt, T, McInnes, IB, Fallon, PG, David, J-P, Liew, FY & Schett, G 2011, 'IL-33 shifts the balance from osteoclast to alternatively activated macrophage differentiation and protects from TNF-alpha-mediated bone loss', J IMMUNOL, vol. 186, no. 11, pp. 6097-105. https://doi.org/10.4049/jimmunol.1003487

APA

Zaiss, M. M., Kurowska-Stolarska, M., Böhm, C., Gary, R., Scholtysek, C., Stolarski, B., Reilly, J., Kerr, S., Millar, N. L., Kamradt, T., McInnes, I. B., Fallon, P. G., David, J-P., Liew, F. Y., & Schett, G. (2011). IL-33 shifts the balance from osteoclast to alternatively activated macrophage differentiation and protects from TNF-alpha-mediated bone loss. J IMMUNOL, 186(11), 6097-105. https://doi.org/10.4049/jimmunol.1003487

Vancouver

Zaiss MM, Kurowska-Stolarska M, Böhm C, Gary R, Scholtysek C, Stolarski B et al. IL-33 shifts the balance from osteoclast to alternatively activated macrophage differentiation and protects from TNF-alpha-mediated bone loss. J IMMUNOL. 2011 Jun 1;186(11):6097-105. https://doi.org/10.4049/jimmunol.1003487

Bibtex

@article{08701c3debd74469844bc2c4bb0164b4,
title = "IL-33 shifts the balance from osteoclast to alternatively activated macrophage differentiation and protects from TNF-alpha-mediated bone loss",
abstract = "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.",
keywords = "Animals, Blotting, Western, Bone Marrow Cells, Bone Resorption, Cell Differentiation, Chondrocytes, Humans, Immunohistochemistry, Interleukins, Macrophages, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Osteoclasts, Receptors, Interleukin, Receptors, Interleukin-1, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Tumor Necrosis Factor-alpha",
author = "Zaiss, {Mario M} and Mariola Kurowska-Stolarska and Christina B{\"o}hm and Regina Gary and Carina Scholtysek and Bartosz Stolarski and James Reilly and Shauna Kerr and Millar, {Neal L} and Thomas Kamradt and McInnes, {Iain B} and Fallon, {Padraic G} and Jean-Pierre David and Liew, {Foo Y} and Georg Schett",
year = "2011",
month = jun,
day = "1",
doi = "10.4049/jimmunol.1003487",
language = "English",
volume = "186",
pages = "6097--105",
journal = "J IMMUNOL",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "11",

}

RIS

TY - JOUR

T1 - IL-33 shifts the balance from osteoclast to alternatively activated macrophage differentiation and protects from TNF-alpha-mediated bone loss

AU - Zaiss, Mario M

AU - Kurowska-Stolarska, Mariola

AU - Böhm, Christina

AU - Gary, Regina

AU - Scholtysek, Carina

AU - Stolarski, Bartosz

AU - Reilly, James

AU - Kerr, Shauna

AU - Millar, Neal L

AU - Kamradt, Thomas

AU - McInnes, Iain B

AU - Fallon, Padraic G

AU - David, Jean-Pierre

AU - Liew, Foo Y

AU - Schett, Georg

PY - 2011/6/1

Y1 - 2011/6/1

N2 - 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.

AB - 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.

KW - Animals

KW - Blotting, Western

KW - Bone Marrow Cells

KW - Bone Resorption

KW - Cell Differentiation

KW - Chondrocytes

KW - Humans

KW - Immunohistochemistry

KW - Interleukins

KW - Macrophages

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Osteoclasts

KW - Receptors, Interleukin

KW - Receptors, Interleukin-1

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Signal Transduction

KW - Tumor Necrosis Factor-alpha

U2 - 10.4049/jimmunol.1003487

DO - 10.4049/jimmunol.1003487

M3 - SCORING: Journal article

C2 - 21515798

VL - 186

SP - 6097

EP - 6105

JO - J IMMUNOL

JF - J IMMUNOL

SN - 0022-1767

IS - 11

ER -