Georg Schett

Universitätsklinikum Erlangen, Erlangen, Bavaria, Germany

Are you Georg Schett?

Claim your profile

Publications (543)3216.78 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: OBJECTIVE: Arthritis is a chronic inflammatory disease characterised by immune cell infiltration and mesenchymal cell expansion in the joints. Although the role of immune cells in arthritis is well characterised, the development of mesenchymal cell hyperplasia needs to be better defined. Here, we analysed the role of the ribosomal S6 kinase Rsk2, which we found to be highly activated in joints of patients with arthritis, in the development of mesenchymal cell hyperplasia. METHODS: We genetically inactivated Rsk2 in the tumour necrosis factor (TNF)-α transgenic (TNFtg) mice, an animal model for human inflammatory arthritis. Clinical and histological signs of arthritis as well as molecular markers of inflammation and joint destruction were quantified. Fibroblast-like synoviocytes (FLS) were characterised in vitro and the effect of Rsk2 deletion on the pattern of gene expression was determined. RESULTS: Rsk2 deficiency in TNFtg mice results in earlier and exacerbated inflammation as well as increased bone and cartilage destruction. The production of inflammatory cytokines, matrix metalloproteinases and osteoclastogenic molecules was significantly increased in vivo upon Rsk2 inactivation. Bone marrow deficient in Rsk2 could not transfer this phenotype, indicating that Rsk2 expression in mesenchymal cells controls the course of arthritis. Indeed, Rsk2 deficiency was associated with a more activated phenotype and higher proliferative capacity of FLS, thereby increasing cytokines and production of matrix proteinases. CONCLUSIONS: Rsk2 emerges as a key regulator of mesenchymal cell numbers in the joint and thereby could be targeted to control the inflammatory and tissue-destructive feature of joints in arthritis. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Annals of the Rheumatic Diseases 11/2014; · 9.11 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In addition to the redundancy of the receptors for the Fc portion of immunoglobulins, glycans result in potential ligands for a plethora of lectin receptors found in immune effector cells. Here we analysed the exposure of glycans containing fucosyl residues and the fucosylated tri-mannose N-type core by complexed native IgG in longitudinal serum samples of well-characterized patients with systemic lupus erythematosus. Consecutive serum samples of a cohort of 15 patients with systemic lupus erythematosus during periods of increased disease activity and remission were analysed. All patients fulfilled the 1982 American College of Rheumatology classification criteria. Sera of 15 sex- and age-matched normal healthy blood donors served as controls. The levels and type of glycosylation of complexed random IgG was measured with lectin enzyme-immunosorbent assays. After specifically gathering IgG complexes from sera, biotinylated lectins Aleuria aurantia lectin and Lens culinaris agglutinin were employed to detect IgG-associated fucosyl residues and the fucosylated tri-mannose N-glycan core, respectively. In sandwich-ELISAs, IgG-associated IgM, IgA, C1q, C3c and C-reactive protein (CRP) were detected as candidates for IgG immune complex constituents. We studied associations of the glycan of complexed IgG and disease activity according to the physician’s global assessment of disease activity and the systemic lupus erythematosus disease activity index 2000 documented at the moment of blood taking. Our results showed significantly higher levels of Aleuria aurantia lectin and Lens culinaris agglutinin binding sites exposed on IgG complexes of patients with systemic lupus erythematosus than on those of normal healthy blood donors. Disease activity in systemic lupus erythematosus correlated with higher exposure of Aleuria aurantia lectin-reactive fucosyl residues by immobilized IgG complexes. Top levels of Aleuria aurantia lectin-reactivity were found in samples taken during the highest activity of systemic lupus erythematosus. Our results show that native circulating IgG complexes from active systemic lupus erythematosus patients expose fucosyl residues and their glycan core is accessible to soluble lectins. Two putative mechanisms may contribute to the increased exposure of these glycans: (1) the canonical N-glycosylation site of the IgG-CH2 domain; (2) an IgG binding non-IgG molecule, like complement or C-reactive protein. In both cases the complexed IgG may be alternatively targeted to lectin receptors of effector cells, e.g. dendritic cells.
    Lupus 11/2014; · 2.78 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In agreement with other autoimmune diseases, systemic sclerosis (SSc) is associated with a strong sex bias. However, unlike lupus, the effects of sex on disease phenotype and prognosis are poorly known. Therefore, we aimed to determine sex effects on outcomes.
    Annals of the rheumatic diseases. 10/2014;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The cornerstone of humoral immunity is the differentiation of B cells into antibody-secreting plasma cells. This process is tightly controlled by a regulatory gene network centered on the transcriptional repressor B lymphocyte-induced maturation protein 1 (Blimp1). Proliferation of activated B cells is required to foster Blimp1 expression but needs to be terminated to avoid overshooting immune reactions. Activator protein 1 (AP-1) transcription factors become quickly up-regulated upon B cell activation. We demonstrate that Fra1, a Fos member of AP-1, enhances activation-induced cell death upon induction in activated B cells. Moreover, mice with B cell-specific deletion of Fra1 show enhanced plasma cell differentiation and exacerbated antibody responses. In contrast, transgenic overexpression of Fra1 blocks plasma cell differentiation and immunoglobulin production, which cannot be rescued by Bcl2. On the molecular level, Fra1 represses Blimp1 expression and interferes with binding of the activating AP-1 member c-Fos to the Blimp1 promoter. Conversely, overexpression of c-Fos in Fra1 transgenic B cells releases Blimp1 repression. As Fra1 lacks transcriptional transactivation domains, we propose that Fra1 inhibits Blimp1 expression and negatively controls plasma cell differentiation through binding to the Blimp1 promoter. In summary, we demonstrate that Fra1 negatively controls plasma cell differentiation by repressing Blimp1 expression.
    Journal of Experimental Medicine 10/2014; · 13.21 Impact Factor
  • Annals of the rheumatic diseases. 10/2014;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: The effect of vitamin D on colorectal adenomas may vary with regard to gender, localisation and histological type of the lesion. AIM: To define the role of vitamin D and gender in a Caucasian cohort of subjects undergoing screening colonoscopy after consideration of established risk factors. METHODS: One thousand five hundred and thirty-two subjects (813 males, 58.8 ± 9.7 years; 719 females, 59.7 ± 10.7 years) were allocated to tertiles of 25-hydroxyvitamin D3 [25(OH)D3 ] serum concentrations. The number, localisation, size and histology of the detected colonic lesions were recorded. RESULTS: Among men, no association was found between vitamin D and the total number, size and histological stage of adenomas at any site. In female subjects, less women with adenomas were found in the highest vitamin D tertile (N = 42/239; 17.2%) as compared to the low vitamin D group (N = 60/240; 25.0%; P = 0.035). In particular, the number of women with adenomas in the proximal colon was significantly lower in the highest tertile (N = 21/239, 8.8%) compared to the low vitamin D group (N = 41/240; 17.1%; P = 0.007). The rates at other sites were not different. The inverse association of vitamin D serum concentrations with the presence of adenomas in the proximal colon was maintained after adjustment for potential confounders. In 80 women on vitamin D supplementation, the rate of adenomas was lower compared to those not on supplementation (3/80; 3.8%; vs. 90/719; 12.5%; P = 0.016). CONCLUSIONS: A potential preventive effect of vitamin D on colorectal adenomas was found in the proximal colon in women. This observation is supported by further decrease of lesions in the proximal colon of women on vitamin D supplementation.
    Alimentary Pharmacology & Therapeutics 10/2014; · 4.55 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objectives. Cardiomyopathy has emerged as a leading cause of death in systemic sclerosis (SSc). However, the pathogenesis of SSc-related cardiomyopathy is poorly understood and new therapies as well as platforms for testing are needed. Here, we aimed to characterize the histopathological features of cardiomyopathy in SSc patients and in common mouse models of SSc.Methods. The histopathological features in myocardial tissues of five patients with SSc and five controls matched for sex, age and cardiovascular risk factors were evaluated and compared to those of three common mouse models of SSc with systemic manifestations: Fra-2 transgenic (Fra-2 tg) mice, mice with sclerodermatous chronic Graft versus Host disease (cGvHD) and tight skin 1 (Tsk-1) mice.Results: Myocardial tissues of SSc patients without clinically manifest cardiac involvement showed endothelial cell apoptosis with reduced capillary density, perivascular inflammation, myofibroblast differentiation and accumulation of collagen. The cGvHD and Tsk-1 models displayed only selected features of SSc-related cardiomyopathy. However, myocardial tissue of Fra-2 tg mice mimicked all features of SSc-related cardiomyopathy and also demonstrated comparable vascular, inflammatory and fibrotic manifestations. Of note, the expression of Fra-2 was also increased in the myocardium of SSc patients.Conclusions. We demonstrate that all typical manifestations of SSc-related cardiomyopathy are mimicked by Fra-2 tg mice. Moreover, the overexpression of Fra-2 in the myocardium of SSc patients may suggest similar underlying pathomechanisms. Thus, Fra-2 tg mice might be a suitable preclinical model to study the mechanisms and therapeutic approaches of myocardial involvement in SSc. \ © 2014 American College of Rheumatology.
    Arthritis & Rheumatology. 10/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Angiogenesis is an important pathophysiological process of chronic inflammation, especially in inflammatory arthritis. Quantitative measurement of changes in vascularization may improve the diagnosis and monitoring of arthritis. The aim of this work is the development of a 3D imaging and analysis framework for quantification of vascularization in experimental arthritis.
    BMC Musculoskeletal Disorders 09/2014; 15(1):298. · 1.88 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: As single cytokine inhibition of e.g. TNFα or IL-6 produces clinically meaningful responses in only about half of RA patients, this study is designed to investigate whether combined inhibition of TNFα and IL-17 has additive/synergistic effects in suppression of mesenchymal cell activation in vitro and inflammation and tissue destruction in arthritis in vivo.Methods: Cultures of human fibroblast-like synoviocytes (FLS) were stimulated with TNFα, IL-17 or a combination of both. Single/combined neutralizing antibodies against TNFα and IL-17 were used to interrogate in vitro cytokine responses and in vivo development of arthritis, bone and cartilage destruction in TNFα-transgenic mice. Bi-specific anti-TNFα/IL-17 antibodies were designed and tested for their potential to block cytokine responses in human FLS.Results: TNFα and IL-17 had additive/synergistic effects in promoting IL-6, -8 and G-CSF as well as MMP production in FLS. Bi-specific anti-TNFα/IL-17 antibodies showed superior efficacy to block cytokine and chemokine responses in vitro. Furthermore, dual versus single inhibition of both cytokines using neutralizing antibodies was more effective in inhibiting the development of inflammation, bone and cartilage destruction in arthritic mice.Conclusion: Combined blockade of TNFα and IL-17 is more effective in inhibiting cytokine, chemokine and matrix enzyme responses from human mesenchymal cells and in blocking tissue destruction associated with arthritis and also showed positive impact on rebalance of bone homeostasis. Bi-specific anti-TNFα/IL-17 antibodies may have superior efficacy in the treatment of arthritis and may overcome the limited therapeutic responses of single cytokine neutralization. © 2014 American College of Rheumatology.
    Arthritis & Rheumatology. 09/2014;
  • Georg Schett, Aline Bozec
    [Show abstract] [Hide abstract]
    ABSTRACT: Osteoporosis results from an imbalance between bone resorption and bone formation. While bone resorption inhibitors are widely used to treat osteoporosis, stimulating bone formation is more challenging. Recently, McClung et al. (2014) found that neutralization of sclerostin, a potent inhibitor of bone formation, effectively increased bone mass in postmenopausal women.
    09/2014; 20(3):394–395.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Sirt1 is a member of the sirtuin family of proteins. Sirt1 is a class III histone deacetylase with important regulatory roles in transcription, cellular differentiation, proliferation and metabolism. As aberrant epigenetic modifications have been linked to the pathogenesis of systemic sclerosis (SSc), we aimed to investigate the role of Sirt1 in fibroblast activation.
    Annals of the Rheumatic Diseases 09/2014; · 9.11 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To assess the efficacy and safety of tocilizumab (TCZ) plus methotrexate/placebo (MTX/PBO) over 2 years and the course of disease activity in patients who discontinued TCZ due to sustained remission.
    Annals of the Rheumatic Diseases 08/2014; · 9.11 Impact Factor
  • Zeitschrift fur Rheumatologie. 08/2014;
  • Bernhard Manger, Georg Schett
    [Show abstract] [Hide abstract]
    ABSTRACT: For patients that present with musculoskeletal symptoms, diagnostic procedures carried out by physicians and rheumatologists are primarily aimed at confirming or excluding the occurrence of primary rheumatic diseases. Another important trigger for musculoskeletal disease, however, is the presence of a tumour. Careful clinical investigation and knowledge of the gestalt of musculoskeletal syndromes related to respective tumour entities is of utmost importance for the diagnosis of paraneoplastic rheumatic diseases such as hypertrophic osteoarthropathy, paraneoplastic polyarthritis, RS3PE syndrome, palmar fasciitis and polyarthritis, cancer-associated myositis and tumour-induced osteomalacia. This places great responsibility on rheumatologists in diagnosing malignancies and referring the patient for effective treatment. The selective influence of tumours on musculoskeletal tissue is surprising and indicates that tumours alter tissues such as the periosteum, synovial membrane, subcutaneous connective tissue, fascia, muscles and bones by specific molecular processes. Some of the underlying mechanisms have been unravelled, providing valuable information on the physiologic and pathophysiologic roles of mediators such as vascular endothelial growth factor and fibroblast growth factor 23.
    Nature Reviews Rheumatology 08/2014; · 9.75 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To determine whether there is an additive effect of anticitrullinated protein antibodies (ACPA) and rheumatoid factor (RF) on the number and size of bone erosions in patients with rheumatoid arthritis (RA) METHODS: 242 patients with RA received high-resolution peripheral quantitative CT (HR-pQCT) scans of the metacarpophalangeal joints. Demographic and disease-specific parameters including ACPA and RF levels were recorded from all patients. Erosion numbers and their size were assessed in 238 patients at 714 individual joints (MCP 2, 3 and 4) and 5712 sites (each 4 quadrants in metacarpal heads and phalangeal bases). The volume of erosions was calculated by a semiellipsoid formula.
    Annals of the rheumatic diseases. 08/2014;
  • Source
    Bernhard Manger, Georg Schett
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective To analyse clinical, laboratory, and imaging characteristics of all patients with palmar fasciitis and polyarthritis syndrome (PFPAS) described in the literature. Method Comparison of the clinical presentation of one patient with acute onset of PFAPS with 99 other published cases identified through a PubMed literature research. Results Since the original description in 1982 by Medsger et al., there have been numerous case reports and small case series in the literature. In total, 73 articles in English, French and Spanish language were included in the analysis. PFPAS is a rare but characteristic paraneoplastic syndrome in rheumatology. Its distinct clinical feature is a painful swelling of both hands caused by an inflammation of the palmar fascia, tendon sheaths, and small joints of fingers und wrist and flexion contractures develop rapidly. Since the subcutaneous tissues become indurated and hard, the illustrative term “woody hands” was coined. The most frequent underlying malignancy is ovarian cancer but adenocarcinomas of the breast, gastrointestinal tract, and other organs can also cause this syndrome. A helpful diagnostic procedure in order to identify the nature of the underlying malignancy in many cases has been the determination of various serum tumour markers. In cases, when a complete removal of the malignancy is possible, PFPAS can also undergo complete remission. Conclusions Knowledge of the distinct features of this rare paraneoplastic syndrome facilitates early diagnosis and potentially life-saving therapeutic interventions.
    Seminars in arthritis and rheumatism 08/2014; · 4.72 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: Nuclear receptors regulate cell growth, differentiation and homeostasis. Selective nuclear receptors promote fibroblast activation, which leads to tissue fibrosis, the hallmark of systemic sclerosis (SSc). Our aim was to investigate the effects of constitutive androstane receptor (CAR/NR1I3), an orphan nuclear receptor, on fibroblast activation and experimental dermal fibrosis.Methods: Expression of CAR was quantified by quantitative PCR, western blot, immunohistochemistry, and immunofluorescence. CAR expression was modulated by small molecules, siRNA, forced overexpression and site-directed mutagenesis. The effects of CAR activation were analyzed in cultured fibroblasts, in bleomycin-induced dermal fibrosis, and in mice overexpressing a constitutively active TGF-β receptor-I (TβRICA).Results: Upregulation of CAR was detected in the skin and in dermal fibroblasts of SSc patients. Stimulation of healthy fibroblasts with TGF-β induced the expression of CAR mRNA and protein in a Smad dependent manner. Pharmacologic activation or overexpression of CAR in healthy fibroblasts significantly increased the stimulatory effects of TGF-β on collagen synthesis and myofibroblast differentiation, and amplified the stimulatory effects of TGF-β on COL1A2 transcriptional activity. Treatment with CAR agonist increased the activation of canonical TGF-β signaling in murine models of SSc and exacerbated bleomycin-induced and TβRICA induced fibrosis with increased dermal thickening, myofibroblasts counts and collagen accumulation.Conclusion: CAR is upregulated in SSc and regulates TGF-β signaling. Activation of CAR increases the profibrotic effects of TGF-β in cultured fibroblasts and in different preclinical models of SSc. Thus, inactivation of CAR might be a novel approach to target aberrant TGF-β signaling in SSc and in other fibrotic diseases. © 2014 American College of Rheumatology.
    Arthritis & Rheumatology. 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective: To investigate the factors associated with cartilage proteoglycan content in patients with rheumatoid arthritis (RA)Methods: 32 RA patients received high-field 3 Tesla Gadolinium-Enhanced MRI of Cartilage (dGEMRIC) for determining cartilage proteoglycan content. Measurements were performed in three individual cartilage regions (medial, central, lateral) of the metacarpophalangeal joints 2 and 3. dGEMRIC values were then related to disease duration, disease activity, anti-citrullinated protein antibody (ACPA) status, rheumatoid factor status and C-reactive protein level.Results: dGEMRIC values were not significantly different between the MCP2 and MCP3 joint. Inter-class correlations were high (>0.92) for all three (medial, central and lateral) cartilage compartments. dGEMRIC values were significantly lower in RA patients with longer disease duration (≥3years) and those with ACPA positivity than those with a short disease duration (<3 years)(p=0.034) or negative ACPA (p=0.0002), respectively. In contrast, no association between cartilage proteoglycan content and disease activity, C-reactive protein level and rheumatoid factor status was found.Conclusion: Decreased cartilage proteoglycan content in RA patients is associated with disease duration and ACPA positivity but not with the actual disease activity, CRP level or rheumatoid factor status. These data suggest that the cumulative burden of inflammation as well as ACPA are the determinants for cartilage damage in RA. © 2014 American College of Rheumatology.
    Arthritis & Rheumatology. 08/2014;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Introduction A major subset of patients with rheumatoid arthritis (RA) is characterised by the presence of circulating autoantibodies directed to citrullinated proteins/peptides (ACPA). These autoantibodies, which are commonly detected using an ELISA assay based on synthetic cyclic citrullinated peptides (CCP), predict clinical onset and a destructive disease course. In the present study, we have utilised plasma and synovial fluids from patients with RA, for the affinity purification and characterisation of anti-CCP2 reactive antibodies, with an aim to generate molecular tools that can be utilized in vitro and in vivo for future investigations into the pathobiology of the ACPA response. Specifically, this study aims to demonstrate that the surrogate marker CCP2 can capture ACPA that bind to autoantigens expressed in vivo, in the major inflammatory lesions of RA, i.e. in the rheumatoid joint. Methods Plasma (n = 16) and synovial fluid (n = 26) samples were collected from RA patients with anti-CCP2 IgG levels above 300 AU/ml. Total IgG was isolated on Protein G columns, and subsequently applied to CCP2 affinity columns. Purified anti-CCP2 IgG was analysed for reactivity and specificity using the CCPlus® ELISA assay, in-house peptide-ELISAs, western blot and immunohisto-/immunocytochemistry. Results Approximately 2 % of the total IgG pool in both plasma and synovial fluid was CCP2-reactive. Purified anti-CCP2 reactive antibodies from different patients showed differences in binding to CCP2 and differences in binding to citrullinated peptides from α-enolase, −vimentin, −fibrinogen, and -collagen type II, illustrating different ACPA fine-specificity profiles. Furthermore, the purified ACPA bound not only in vitro citrullinated proteins but more importantly, in vivo-generated epitopes on synovial fluid cells and synovial tissues from RA patients. Conclusions We have isolated ACPA from plasma and synovial fluid, and demonstrated that the CCP2 peptides, frequently used in diagnostic ELISA assays, de facto act as surrogate antigens for at least four different, well-characterised, largely non cross-reactive, ACPA fine-specificities. Moreover, we have determined the concentration and proportion of CCP2-reactive IgG molecules in rheumatoid plasma and synovial fluid, and we have shown that the purified ACPA can be used to detect both in vitro- and in vivo-generated citrullinated epitopes by various techniques. We anticipate that these antibodies will provide us with new opportunities to investigate the potential pathogenic effects of human ACPAs.
    Arthritis research & therapy 07/2014; · 4.27 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objectives: Both psoriatic arthritis (PSA) and hand osteoarthrits (HOA) lead to periarticular bone proliferation. Aim of this study was to investigate the different patterns of bony spur formation in PSA and HOA by high-resolution peripheral quantitative computed tomography (HR-pQCT).Methods: 70 patients, 25 with PSA, 25 with HOA and 20 healthy controls, with similar age and sex distribution and clinical involvement of the metacarpophalangeal (MCP) joints received a HR-pQCT examination of the MCP 2, 3 and 4 joint of the dominantly affected hand. Demographic and disease-specific data were recorded and number, size and distribution of bony spur were assessed and compared between PsA and HOA.Results: Overall number and size of bony spurs was similar between PsA and HOA. PsA and HOA, however, substantially differed in the localization of lesions within individual joints: Bony spurs in PsA dominated the radial sides of the joints (PsA vs. HOA: metacarpal head 2: p<0.001; phalangeal base 2: p<0.001), whereas the palmar and dorsal sites were the predilection sites in HOA. Detailed anatomical analysis showed that enthesial regions are almost exclusively affected in PsA, but are spared in HOA, whereas bony spurs in HOA typically emerge at the cartilage-bone interphase and the joint margins.Conclusions: Our findings suggest a similar burden of bony spurs in PsA and HOA. Nonetheless, the anatomical sites of bony proliferation in PsA and HOA are different between PsA and HOA. © 2014 American College of Rheumatology.
    Arthritis & Rheumatology. 07/2014;

Publication Stats

11k Citations
3,216.78 Total Impact Points

Institutions

  • 2007–2014
    • Universitätsklinikum Erlangen
      • Institute of Human Genetics
      Erlangen, Bavaria, Germany
    • Justus-Liebig-Universität Gießen
      • Department of Internal Medicine
      Gieben, Hesse, Germany
  • 2006–2014
    • Friedrich-Alexander Universität Erlangen-Nürnberg
      • • Nikolaus-Fiebiger-Center of Molecular Medicine (NFZ)
      • • Department of Biology
      Erlangen, Bavaria, Germany
  • 2013
    • Inselspital, Universitätsspital Bern
      • Department of Rheumatology, Clinical Immunology and Allergology
      Bern, BE, Switzerland
    • University of Leeds
      • Leeds Institute of Rheumatic and Musculoskeletal Medicine
      Leeds, England, United Kingdom
  • 1998–2013
    • Medical University of Vienna
      • Department of Medicine II
      Wien, Vienna, Austria
  • 1996–2013
    • University of Innsbruck
      • Institute of Biochemistry
      Innsbruck, Tyrol, Austria
  • 2012
    • Nordic Bioscience
      København, Capital Region, Denmark
    • Universitair Ziekenhuis Leuven
      Louvain, Flanders, Belgium
    • Ghent University
      • Rheumatology
      Gent, VLG, Belgium
    • Ludwig Boltzmann Institute for Osteology
      Wien, Vienna, Austria
  • 2008–2012
    • University of Zurich
      • Center for Integrative Human Physiology
      Zürich, ZH, Switzerland
    • Technische Universität Dresden
      Dresden, Saxony, Germany
  • 2006–2012
    • Medizinische Universität Innsbruck
      • • Department für Innere Medizin
      • • Univ.-Klinik für Neurologie
      Innsbruck, Tyrol, Austria
  • 2011
    • Università degli studi di Parma
      Parma, Emilia-Romagna, Italy
    • National Academy of Sciences of Ukraine
      • Institute of Cell Biology
      Kharkiv, Kharkivs'ka Oblast', Ukraine
  • 2007–2011
    • University of Glasgow
      • • College of Medical, Veterinary and Life Sciences
      • • Institute of Infection, Immunity and Inflammation
      Glasgow, SCT, United Kingdom
  • 2010
    • Detská fakultná nemocnica s poliklinikou v Bratislave
      Presburg, Bratislavský, Slovakia
    • Comenius University in Bratislava
      Presburg, Bratislavský, Slovakia
  • 2009
    • University of California, San Diego
      • Division of Rheumatology, Allergy and Immunology
      San Diego, CA, United States
    • Universitätsklinikum Jena
      Jena, Thuringia, Germany
  • 1998–2008
    • University of Vienna
      • • Department of Internal Medicine III
      • • Department of Pharmacology and Toxicology
      • • Universitätsklinik für Innere Medizin I
      Wien, Vienna, Austria
  • 2004–2006
    • Biomedical Sciences Research Center Alexander Fleming
      • Institute of Immunology
      Βάρη, Attica, Greece
  • 2000
    • Vienna General Hospital
      Wien, Vienna, Austria
  • 1995–2000
    • Austrian Academy of Sciences
      • Institut für Biomedizinische Alternsforschung
      Vienna, Vienna, Austria
  • 1998–1999
    • Ludwig Boltzmann Institute of Rheumatology and Balneology
      Wien, Vienna, Austria