958 Scientific Abstracts References: [1] Bennet RG. Relaxin and its role in the development and treatment of fibrosis. Transl Res 2009;145:1-6. [2] Khanna D, Clements PJ, Furst DE, Korn JH, Ellman M, Rothfield N, Wigley FM, Moreland LW, Silver R, Kim YH, Steen VD, Firestein GS, Kavanaugh AF,Weisman M, Mayes MD, Collier D, Csuka ME, Simms R, Merkel PA, Medsger TA Jr, Sanders ME, Maranian P, Seibold JR; Relaxin Investigators and the Scleroderma Clinical Trials Consortium. Recombinant human relaxin in the treatment of systemic sclerosis with diffuse cutaneous involvment: a randomized, double-blind, palcebo-controlled trial. Arthritis Rheum 2009;60:1102-1111. Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2015-eular.5458 AB0201 ALTERED SERUM FATTY ACID PROFILES IN PATIENTS WITH POLYMYOSITIS OR DERMATOMYOSITIS COMPARED TO HEALTHY INDIVIDUALS AND IN RELATION TO IMMUNOSUPPRESSIVE TREATMENT J. Raouf 1 , H. Idborg 1 , P. Olsson 2 , P.-J. Jakobsson 1 , I.E. Lundberg 1 , M. Korotkova 1 . 1 Medicine, Karolinska Institutet; 2 Analytical Chemistry, Stockholm University, Stockholm, Sweden Background: Polymyositis (PM) and dermatomyositis (DM) are chronic autoim- mune diseases, characterized by muscle fatigue and low muscle endurance. Histopathological characteristics of muscle biopsies are infiltration of inflamma- tory cells, muscle fiber degeneration and regeneration. Conventional treatment includes high doses of glucocorticoids and immunosuppressive drugs, however, only a limited number of patients recover muscle function. Our group has recently found that immunosuppressive treatment has significant effects on gene expression related to lipid and fatty acid (FA) metabolism that may contribute to the persistent muscle weakness often seen in myositis patients. Lipid dysregulation might lead to generation of lipotoxic mediators which contribute to cell dysfunction or death. Furthermore, a number of studies have confirmed the important effects of FA on skeletal muscle growth, strength and inflammation. However the involvement of lipids and FA in the pathogenesis of polymyositis and dermatomyositis has not been clarified. Objectives: To analyze lipid and FA profiles in sera from patients with polymyositis or dermatomyositis in comparison to healthy individuals and in relation to immunosuppressive treatment. Methods: Serum samples were obtained from 14 patients with established PM or DM and 12 healthy individuals. Serum lipids were extracted by using liquid-liquid extraction (LLE). FA composition of total lipids was determined by gas chromatography flame ionization detector (GC-FID). FA composition of several lipid classes e.g., triacylglycerols, phospholipids, sphingolipids and lysophospholipids was analyzed by using liquid chromatography tandem mass spectrometry (LC-MS/MS). In addition, serum samples from 8 myositis patients before and after 6 months of immunosuppressive treatment was extracted by LLE and analyzed by LC-MS/MS. Results: Our preliminary results suggest that FA composition of total serum lipids was different in myositis patients compared to healthy donors; the levels of palmitic16:0 acid was significantly higher (<0.05) in myositis patients whereas the levels of arachidonic 20:4 (n-6) acid was significantly lower (p=0.05). Immunosuppressive treatment did not affect the total levels of lipid classes in the serum from myositis patients. However, the levels of phosphatidylcholine (PC) PC (32:1), phosphatidylethanolamine (PE) PE (36:5) and lysophosphatidylcholine (LPC) LPC (16:1) were all significantly higher (p<0.05) in myositis patients after 6 months of immunosuppressive treatment. Conclusions: FA composition of total serum lipids is altered in myositis patients compared to healthy controls. Immunosuppressive treatment resulted in changed FA composition of serum PC, PE and LPC. These findings indicate that FA metabolism might be deregulated in PM and DM patients and may be further affected by immunosuppressive treatment. Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2015-eular.5065 AB0202 GALECTIN-9 IS A ROBUST BIOMARKER FOR DISEASE ACTIVITY IN JUVENILE DERMATOMYOSITIS AND ACTS AS A T CELL ACTIVATOR F. Bellutti Enders 1,2 , J. Wienke 2 , W. de Jager 2 , L. Wedderburn 3 , K. Nistala 3 , C. Pilkington 3 , B. Prakken 2 , A. van Royen-Kerkhof 2 , F. van Wijk 2 . 1 Pediatrics, Centre Hospitalier Universitaire Vaudois, University hospital, Lausanne, Switzerland; 2 Pediatric immunology, Laboratory of translational immunology, UMC Utrecht, Utrecht, Netherlands; 3 Pediatric rheumatology, UCL Institute of Child Health, London, United Kingdom Background: Juvenile dermatomyositis (JDM) is a rare, but severe chronic systemic autoimmune disease in children, characterized by muscle weakness and a typical skin rash. Clinical evaluation of disease activity remains challenging. Recently, we identified a protein that highly correlates with disease activity in a Dutch JDM cohort: galectin-9 (gal-9). The immunobiological role of gal-9 in autoimmune diseases is still controversial. On the one hand it is known for its immunosuppressive effects by inducing apoptosis in T-helper (Th) 1 and Th17 cells and activating regulatory T cells, on the other hand it has been implicated in T cell activation and Th1 skewing. Objectives: To validate the potential of gal-9 as a biomarker in JDM and investigate its immunobiological effects on T cell skewing and activation. Methods: Gal-9 was measured in patient’s serum of an independent JDM cohort by multiplex immunoassay. For functional experiments, naive CD4 T cells were isolated and stimulated with different concentrations of gal-9, plus anti-CD3 and antigen presenting cells. To test specificity, a gal-9 blocking agent (TIM-3 fusion protein) as well as a control from the galectin family (galectin-8) were included. Flow cytometric analysis of proliferation and T cell activation markers was performed on day 3 and 5 of culture. Cytokines TNFα, IFNγ, IL-13, IL-17 and IL-10 were measured in the culture supernatants of days 3, 5 and 7 by multiplex immunoassay. Results: Measurement of gal-9 in serum confirmed its high discriminative value for active disease versus remission (P=.0001; AUC 0.894; OR 9.17) even under medication, as well as a strong correlation with the clinical disease activity scores CMAS and Physician’s Global VAS. On a functional level, the presence of gal-9 induced a slight but significant increase in naive CD4 T cell proliferation after 3 days of culture. The T cell activation markers CD25, CD69 and TIM-3 showed the same pattern. Gal-9 also increased production of IFNγ, TNFα and IL-10, mainly at day 7. These effects were not seen in the control conditions. Conclusions: We confirmed the potential use of a very robust biomarker, galectin-9, that highly correlates with disease activity in juvenile dermatomyositis. Introduction of this biomarker into clinical practice will help to personalize treatment. Functionally, we found that gal-9 is a T cell activator, causing increased proliferation, cytokine production and expression of T cell activation markers. The high levels of circulating gal-9 in JDM patients may therefore contribute to the immunopathogenesis of JDM. References: [1] Bellutti Enders et al. Correlation of CXCL10, TNFRII, and Galectin-9 With Disease Activity in Juvenile Dermatomyositis. Arthritis Rheumatol. 2014 Aug;66(8):2281-9. Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2015-eular.4858 AB0203 POSSIBLE ROLE OF FRACTALKINE/CX3CL1 (FKN) IN THE MICROVASCULAR DAMAGE OF SYSTEMIC SCLEROSIS (SSC) K. Stefanantoni 1 , I. Sciarra 1 , C. Corinaldesi 2 , M. Caucci 1 , M. Vasile 1 , N. Iannace 1 , M.C. Saturno 1 , C. Crescioli 2 , G. Valesini 1 , V. Riccieri 1 . 1 Dipartimento di Medicina Interna e Specialità Mediche-Reumatologia, Sapienza Università di Roma; 2 Dipartimento di Scienze Motorie, Umane e della Salute, Università degli studi di Roma “Foro Italico”, Rome, Italy Background: Systemic Sclerosis (SSc) is a severe autoimmune disease charac- terized by tissue fibrosis, immune dysregulation and vascular dysfunction. Nailfold Videocapillaroscopy (NVC) is a simple diagnostic tool that is commonly used to assess microvascular changes in SSc (1). Fractalkine/CX3CL1 (FKN) is a member of CX3C chemokine family and is expressed on tumor necrosis factor α (TNF-α) and IL-1 stimulated endothelial cells (2,3). In SSc it seems to be expressed on endothelial cells in the affected skin and in lung tissue and raised serum levels of FKN are associated with higher erythrocyte sedimentation rates, presence of digital ischemia, and severity of pulmonary fibrosis (4) and pulmonary arterial hypertension (5). Objectives: To assess the role of Fractalkine/CX3CL1 in the development of the different capillaroscopic patterns in SSc.