IL-33 exacerbates antigen-induced arthritis by activating mast cells

Xu, Damo; Jiang, Hui-Rong; Kewin, Peter; Li, Yubin; Mu, Rong; Fraser, Alasdair R.; Pitman, Nick; Kurowska‐Stolarska, Mariola; McKenzie, Andrew N. J.; McInnes, Iain B.; Liew, Foo Y.

doi:10.1073/pnas.0801898105

Cited by 428 publications

(500 citation statements)

References 37 publications

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“…DBA/1 mice deficient in IFN␥ or its receptor were found to be highly susceptible to the development of CIA (6). More recently described cytokines such as IL-17, IL-21, IL-23, IL-32, and IL-33 have all been reported to aggravate CIA (11,12).…”

Section: Animal Models Of Rheumatoid Arthritismentioning

confidence: 99%

Evaluation of therapeutic targets in animal models of arthritis: How does it relate to rheumatoid arthritis?

Bevaart¹,

Vervoordeldonk²,

Tak³

2010

Arthritis & Rheumatism

228

193

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There are accumulating data describing the association between diabetes and cancer mortality from Westernised populations. There are no data describing the relationship between diabetes and cancer mortality in African or South Asian populations from developing countries. We explored the relationship of abnormal glucose tolerance and diabetes on cancer mortality risk in a large, multi‐ethnic cohort from the developing nation of Mauritius. Population‐based surveys were undertaken in 1987, 1992 and 1998. The 9559 participants comprised 66% of South Asian (Indian), 27% of African (Creole), and 7% of Chinese descent. Cox's proportional hazards model with time varying covariates was used to obtain hazard ratios (HRs) and 95% confidence intervals (95% CI) for risk of cancer mortality, after adjustment for confounding factors. In men, but not women, cancer mortality risk increased with rising 2h‐PG levels with HR for the top versus bottom quintile of 2.77 (95%CI: 1.28 to 5.98). South Asian men with known diabetes had a significantly greater risk of cancer mortality than those with normal glucose tolerance (NGT) HR: 2.74 (95%CI: 1.00‐7.56). Overall, impaired glucose tolerance was associated with an elevated risk of cancer mortality compared to NGT (HR: 1.47, 95% CI: 0.98–2.19), though this was not significant. We have shown that the association between abnormal glucose tolerance and cancer extends to those of African and South Asian descent. These results highlight the importance of understanding this relationship in a global context to direct future health policy given the rapid increase in type 2 diabetes, especially in developing nations.

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Section: Animal Models Of Rheumatoid Arthritismentioning

confidence: 99%

Evaluation of therapeutic targets in animal models of arthritis: How does it relate to rheumatoid arthritis?

Bevaart¹,

Vervoordeldonk²,

Tak³

2010

Arthritis & Rheumatism

228

193

View full text Add to dashboard Cite

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“…The doses of rIL-33 used in these experiments were biologically effective, as they were able to induce IL-6 and IL-13 secretion by bone marrow-derived mast cells (data not shown), consistent with what has previously been described. 29 …”

Section: Epithelial-derived Uv-induced Skin Tumors That Evade Immunolmentioning

confidence: 99%

“…28 Similar to the effects of UV, IL-33 has potent immunemodulating properties that are mediated by the induction of cytokines including IL-1, -4, -6, -10. and -13, as well as chemokines such as CXCL8, CCL2, CCL3, and CCL5. 22,23,29,30 Consequently, although IL-33 can reduce the development of atheroscleoris 31 and prevent the development of parasitic-induced encephalitis, 32 it may also promote the development of asthma 33 and ar-thritis. 29 Recently, the immune-modulating functions of IL-33 have been extended to include attenuation of bacterial sepsis via neutrophil recruitment 28 and the activation of newly discovered "nuocytes" for the effective elimination of parasitic infections.…”

mentioning

confidence: 99%

The Immune-Modulating Cytokine and Endogenous Alarmin Interleukin-33 Is Upregulated in Skin Exposed to Inflammatory UVB Radiation

Byrne

Beaugie

O’Sullivan

et al. 2011

The American Journal of Pathology

103

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The cellular and molecular mechanisms by which UV radiation modulates inflammation and immunity while simultaneously maintaining skin homeostasis is complex and not completely understood. Similar to the effects of UV, IL-33 has potent immune-modulating properties that are mediated by the downstream induction of cytokines and chemokines. We have discovered that exposure of mice in vivo or human skin samples ex vivo to inflammatory doses of UVB induced IL-33 expression within the epidermal and dermal skin layers. Using a combination of murine cell lines and primary human cells, we demonstrate that both UV and the oxidized lipid platelet activating factor induce IL-33 expression in keratinocytes and dermal fibroblasts. Highlighting the significance of these results, we found that administering IL-33 to mice in vivo suppressed the induction of Th1-mediated contact hypersensitivity responses. This may have consequences for skin cancer growth because UV-induced squamous cell carcinomas that evade immunological destruction were found to express significantly higher levels of IL-33. Finally, we demonstrate that dermal mast cells and skininfiltrating neutrophils closely associate with UV-induced IL-33-expressing fibroblasts. Our results therefore identify and support a role for IL-33 as an important early danger signal produced in response to inflammation-inducing UV radiation.

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“…Mice administered intra-articularly with bovine serum albumin exhibited hypernociception which was blocked by sST2 [33]. In addition, IL-33 was recently shown to exacerbate antigen-induced arthritis by activating bone marrow-derived mast cells [34], and administration of a blocking anti-ST2 antibody attenuated the severity of collagen-induced arthritis [22,35].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2011

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1 IL-33 is expressed in human osteoblasts, but has no direct effect on bone remodelingsuggested that expression of IL-33, in contrast to that of IL-1β, is not repressed by PPARγ, likely explaining why IL-33, but not IL-1β, is expressed in adipocytes. The IL-33 receptor ST2L is not constitutively expressed in human bone marrow stromal cells, osteoblasts or CD14-positive monocytes, and IL-33 has no effect on these cells. In addition, although ST2L mRNA is induced by TNF-α and IL-1β in bone marrow stromal cells, IL-33 has the same effects as TNF-α and IL-1β, and, therefore, the biological activity of IL-33 may be redundant in this system. In agreement with this hypothesis, MC3T3-E1 osteoblast-like cells constitutively express ST2L mRNA, and in these cells IL-33 and TNF-α/IL-1β similarly decrease osteocalcin RNA levels in these cells. In conclusion, our results suggest that IL-33 has no direct effects on normal bone remodeling.

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IL-33 exacerbates antigen-induced arthritis by activating mast cells

Cited by 428 publications

References 37 publications

Evaluation of therapeutic targets in animal models of arthritis: How does it relate to rheumatoid arthritis?

Evaluation of therapeutic targets in animal models of arthritis: How does it relate to rheumatoid arthritis?

The Immune-Modulating Cytokine and Endogenous Alarmin Interleukin-33 Is Upregulated in Skin Exposed to Inflammatory UVB Radiation

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

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