ACR Meeting Abstracts

ACR Meeting Abstracts

Abstract Number: 1766

Role Of IL33 In The Inflammation Of Takayasu Arteritis

David Saadoun1, Marlène Garrido2, Julien Gaudric3, Cloé Comarmond4, Michele Rosenzwacjg5 and Patrice Cacoub6, 1Groupe Hospitalier Pitié Salpétrière, Service de Médecine Interne, DHU i2B, Paris, France, 2I3 laboratory, Pitié-Salpétrière, Paris, France, 3Department of Vascular surgery GHPS, Paris, France, 4Internal Medicine and Clinical Imunology, Referal Center for Autoimmune diseases, Internal Medicine and Clinical Imunology, Hôpital Pitié Salpétrière, Paris, France, 5Department of Immunology GHPS, Paris, France, 6Médecine Interne 2, Hopital Pitié-Salpétrière, Paris, France

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: , ,

Session Information

Title: Cytokines, Mediators, Cell-cell Adhesion, Cell Trafficking and Angiogenesis II: Mechanisms that contribute to autoimmune inflammation

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Interleukin (IL)-33, a member of the IL-1 cytokine family, is a recently described novel activator of endothelial cells, which promotes adhesion molecules and proinflammatory cytokine expression in the endothelium and angiogenesis and vascular permeability. Unlike, the other IL-1 family members, IL-33 primarily induces T-helper (Th)2 immune responses and the polarisation of macrophages.

Objective: To analyse the role of IL-33 and its receptor ST2 in the pathogenesis of Takayasu arteritis (TA).

Methods:

Thirty three TA patients fulfilling the ACR criteria, with active disease (aTA) or inactive disease (iTA) and 10 age-matched controls (HD) were included. We performed quantitative measurement of IL-33, analysis of cell surface markers and cytokine production by flow cytometry and Luminex. Immunohistochemical analysis of inflamed aorta from patients with TA was performed.

Results:

Increased level of serum (mean ± SEM; 155 ± 69.5 vs 32.9 ± 19.6 pg/ml, respectively, p=0.040) and culture supernatants IL-33 (14.6± 3.3 vs 2.9 ±1.8 pg/ml, respectively, p=0.013) was observed in TA patients compared to HD. Level of IL-33 correlated with disease activity in TA patients (25.4± 6.5 in aTA vs 7.5 ±2.6 pg/ml in iTA, p=0.021) and with the NIH score (r2=0.3009, p=0.0009). IL-33 level dropped in active TA patients (n=10) that become inactive (20.1± 6.7 vs 4.2 ±1.2 pg/ml, p=0.031). IL-33 was mainly produced by eosinophils, basophils, and mast cells and in a lesser extent by macrophages and CD8+ T cells. ST2 (i.e. the IL-33 receptor) was mainly expressed by eosinophils and mast cells and much weaker by macrophages and neutrophils. IL-33 and ST2 were overexpressed in the inflamed arteries of TA patients and colocalized with endothelial cells and T cells, respectively. Stimulation of purified CD4+ T cells with IL-33 increased Th2 cells.

Conclusion:

These findings open new perspectives for the role of IL-33 in the pathogenesis of TA.

Disclosure:

D. Saadoun,
None;

M. Garrido,
None;

J. Gaudric,
None;

C. Comarmond,
None;

M. Rosenzwacjg,
None;

P. Cacoub,
None.

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