G S Panayi

King's College London, Londinium, England, United Kingdom

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Publications (377)1971.18 Total impact

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    ABSTRACT: Background Rasolvir (BiP) is a human endoplasmic reticulum-resident stress protein. In pre-preclinical studies it has prolonged anti-inflammatory properties by the induction of regulatory cells. A single intravenous infusion suppresses ongoing collagen-induced arthritis in the mouse; ameliorates arthritis and inhibits bone damage in the TNFa-trangenic mouse; and suppresses inflammation in the RA synovial membrane/SCID transplantation model (see review). It is thus a potential new therapy for RA acting by a novel mode of action. Objectives The objectives of this randomised placebo-controlled, dose ascending double blind Phase I/IIA trial of Rasolvir were safety (Primary Objective) and efficacy as measured by the DAS28 (Secondary Objective). Methods Forty-one patients with established active RA, who had failed DMARDs, were assessed; 24 fulfilled the inclusion/exclusion criteria. They were sequentially assigned to three cohorts each of 8 patients randomly allocated to receive placebo (2 patients) or Rasolvir (6 patients). Patients received a single intravenous infusion over 1hr and observed as inpatients overnight. Cohort 1 received 1mg rasolvir; 2 5mg; and 3 15mg. No patients were re-treated. Clinical, rheumatological and laboratory assessments for safety and efficacy (DAS28) were carried out at stated intervals for 12 weeks. Results SAFETY. No infusion reactions or serious adverse reactions were noted. Adverse events were evenly distributed between placebo and IMP groups demonstrating no Rasolvir-related toxicity. Haematological, renal and metabolic parameters remained within the normal range. EFFICACY. Six patients receiving placebo and 6 in each Rasolvir group were available for analysis. Although the placebo group had a high frequency of moderate EULAR responses, the highest rate of EULAR good responses was observed in the Rasolvir groups. Good EULAR responses were seen as early as 3 weeks after the infusion. At 12 weeks, 3 patients who had received Rasolvir were still in remission (DAS28 ≤2.6). Conclusions Rasolvir is safe when administered up to a dose of 15mg in patients with active RA. A higher rate of good EULAR response after a single dose of Rasolvir suggests that it merits further study as a treatment447855328407 of RA. References Acknowledgements Study funded by Arthritis Research UK. Support received from the Biomedical Research Centre KCL; Quintiles for the infusion and overnight stay; Kings Health Partners Joint Clinicat Trials Office; the Pharmacy at GSTT. The Rasolvir produced at CBC, Bristol University. Disclosure of Interest B. Kirkham Grant/research support from: AbbVie;UC, Consultant for: Novartis; AbbVie; BMS; Lilly; MSD, Speakers bureau: BMS; MSD; UCB, K. Chaabo: None declared, C. Hall: None declared, A. Vincent: None declared, J. Vasconcelos: None declared, T. Prevost: None declared, G. Panayi Shareholder of: Immune Regulation Ltd, V. Corrigall Shareholder of: Immune Regulation Ltd
    Annals of the Rheumatic Diseases 06/2015; 74(Suppl 2):480.2-481. DOI:10.1136/annrheumdis-2015-eular.3346 · 10.38 Impact Factor
  • Gabriel S Panayi · Valerie M Corrigall ·
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    ABSTRACT: Immunoglobulin heavy-chain-binding protein (BiP) or glucose-regulated protein 78 (Grp78) is a vital ubiquitous resident of the endoplasmic reticulum (ER). As an intracellular chaperone, BiP correctly folds nascent polypeptides within the ER and regulates the unfolded protein response ensuring protection of the cell from denatured protein and reinforcing its anti-apoptotic role, when the cell is under stress. Additionally, BiP is a member of the heat-shock protein (HSP) 70 family and, as a stress protein, is up-regulated by conditions of reduced oxygen and glucose. Cell stress induces surface expression and secretion of BiP. Consequently, BiP is detectable in several bodily fluids including serum, synovial fluid (SF) and oviductal fluid. However, as an extracellular protein, BiP has additional properties that are quite distinct from the intracellular functions. Extracellular BiP is immunoregulatory and anti-inflammatory causing development of tolerogenic dendritic cells (DCs), induction of regulatory T-cells, abrogation of osteoclast development and function, induction of anti-inflammatory cytokine production, including interleukin (IL)-10, IL-1 receptor antagonist and soluble tumour necrosis factor (TNF)-receptor type II, and attenuation of TNFα and IL-6. Together, these functions help drive the resolution of inflammation. Disease models of inflammatory arthritis have helped to demonstrate the novel mode of action of BiP in which the pharmacokinetics and pharmacodynamics are dissociated. The three murine models to be discussed each show BiP induced long-term therapeutic protection and therefore has potential for long-lasting drug-free therapy in rheumatoid arthritis (RA).
    Biochemical Society Transactions 12/2014; 42(6):1752-5. DOI:10.1042/BST20140230 · 3.19 Impact Factor
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    ABSTRACT: Recombinant human binding immunoglobulin protein (BiP), has previously demonstrated anti-inflammatory properties in multiple models of inflammatory arthritis. We investigated whether these immunoregulatory properties could be exploited using gene therapy techniques. A single intraperitoneal injection of lentiviral vector containing the murine BiP (Lenti-mBiP) or green fluorescent protein (Lenti-GFP) transgene, was administered in low or high dose studies during early arthritis. Disease activity was assessed by visual scoring, histology, serum cytokine and antibody production measured by cell ELISA and ELISA respectively. Lentiviral vector treatment caused significant induction of IFNγ responses regardless of the transgene, however further specific effects were directly attributable to the BiP transgene. In both studies Lenti-mBiP significantly suppressed clinical arthritis. Histological examination showed that low dose Lenti-mBiP suppressed inflammatory cell infiltration, cartilage destruction and significantly reduced pathogenic anti-CII antibodies. Lenti-mBiP treatment caused significant upregulation of soluble cytotoxic T lymphocyte antigen-4 (sCTLA-4) serum levels and downregulation of IL-17A production in response to type II collagen (CII) cell restimulation. In vitro studies confirmed that Lenti-mBiP spleen cells could significantly suppress the release of IL-17A from CII primed responder cells following CII restimulation in vitro and this suppression was associated with increased IL-10 production. Neutralisation of CTLA-4 in further co-culture experiments demonstrated inverse regulation of IL-17A production. In conclusion, these data demonstrate proof of principle for the therapeutic potential of systemic lentiviral vector delivery of the BiP transgene leading to immunoregulation of arthritis by induction of soluble CTLA-4 and suppression of IL-17A production.
    Clinical & Experimental Immunology 09/2014; 179(2). DOI:10.1111/cei.12456 · 3.04 Impact Factor
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    ABSTRACT: Objective Type II collagen (CII) posttranslationally modified by reactive oxygen species (ROS-CII) that are present in the inflamed joint is an autoantigen in rheumatoid arthritis (RA). The aim of this study was to investigate the potential use of anti-ROS-CII autoantibodies as a biomarker of RA. MethodsCII was exposed to oxidants that are present in the rheumatoid joint. Autoreactivity to ROS-CII was assessed by enzyme-linked immunosorbent assays in synovial fluid (SF) and serum samples obtained from patients during various phases of RA. This group included disease-modifying antirheumatic drug (DMARD)-naive patients with early RA (n = 85 serum samples) and patients with established RA (n = 80 serum and 50 SF samples), who were categorized as either DMARD responders or DMARD nonresponders. Control subjects included anti-citrullinated protein antibody (ACPA)-positive patients with arthralgia (n = 58 serum samples), patients with osteoarthritis (OA; n = 49 serum and 52 SF samples), and healthy individuals (n = 51 serum samples). ResultsReactivity to ROS-CII among DMARD-naive patients with early RA was significantly higher than that among patients with ACPA-positive arthralgia, patients with OA, and healthy control subjects (P < 0.0001), with 92.9% of serum samples from the patients with early RA binding to anti-ROS-II. There was no significant difference in anti-ROS-CII reactivity between ACPA-positive and ACPA-negative patients with RA, with 93.8% and 91.6% of serum samples, respectively, binding to ROS-CII. The sensitivity and specificity of binding to ROS-CII in patients with early RA were 92% and 98%, respectively. Among patients with established RA, serum reactivity in DMARD nonresponders was significantly higher than that in DMARD responders (P < 0.01); 58.3% of serum samples from nonresponders and 7.6% of serum samples from responders bound to HOCl-ROS, while the respective values for SF were 70% and 60%. In patients with longstanding RA, autoreactivity to ROS-CII changed longitudinally. Conclusion Autoantibodies to ROS-CII have the potential to become diagnostic biomarkers of RA.
    Arthritis & Rheumatology 07/2013; 65(7). DOI:10.1002/art.37964 · 7.76 Impact Factor
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    GS Panayi · M Bodman-Smith · M Fife · V Corrigall · D Pappin · J Lanchbury ·

    Arthritis Research & Therapy 04/2012; 1:1-1. DOI:10.1186/ar21 · 3.75 Impact Factor
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    Adrian M Shields · Gabriel S Panayi · Valerie M Corrigall ·
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    ABSTRACT: Heat shock proteins (HSPs) and other members of the much broader stress protein family have been shown to play important roles in coordinating multiple phases of immunological reactions; from facilitating immunological recognition, to promoting and regulating immunological responses and finally augmenting the resolution of inflammation and return to immunological homeostasis. In this review, we consider the challenges facing the stress protein field as we enter 2012; in particular we consider the role that HSPs and stress proteins may play in the initiation and termination of immunological responses. Special attention is afforded to the resolution-associated molecular pattern, binding immunoglobulin protein (BiP, also known as glucose regulated protein-78). We review the evidence that resolution-promoting proteins such as BiP may herald a new generation of biologics for inflammatory disease and reflect on the challenges of achieving clinical remission in rheumatoid arthritis with novel therapeutics and correlating clinical remission with immunological parameters of resolution of inflammation.
    Frontiers in Immunology 02/2012; 3:17. DOI:10.3389/fimmu.2012.00017
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    Rheumatology (Oxford, England) 01/2012; 51(4):759-61. DOI:10.1093/rheumatology/ker399 · 4.48 Impact Factor
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    ABSTRACT: Appropriate regulation and subsequent resolution of acute inflammatory events is critical to the prevention of autoinflammatory diseases. Indeed, the chronic inflammation observed in diseases such as RA is at least partially consequent on the failure of endogenous immunoregulation. Current RA therapies (e.g. anti-TNF-α inhibitors and MTX) inhibit components of the inflammatory disease process without directly promoting the resolution of inflammation. We propose that the next generation of RA therapeutics will complement and augment endogenous immunoregulatory and pro-resolution immunological networks, thus promoting the definitive resolution of inflammation rather than temporary immunological control. Of particular interest with respect to this therapeutic approach is binding immunoglobulin protein [BiP; also known as glucose-regulated protein-78 (GRP78)], a member of the recently defined resolution-associated molecular pattern (RAMP) family of molecules. In this review, we consider the preclinical evidence from experiments in mouse and man that suggests BiP and other members of the RAMP family have the potential to herald a new generation of immunotherapeutics.
    Rheumatology (Oxford, England) 12/2011; 51(5):780-8. DOI:10.1093/rheumatology/ker412 · 4.48 Impact Factor
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    ABSTRACT: Binding immunoglobulin protein (BiP) has previously shown powerful anti-inflammatory properties in the collagen-induced arthritis (CIA) model, where a single dose of BiP has proved to be both a long-term prophylactic and therapeutic. In both CIA and human in vitro studies, BiP induced regulatory T cells. The present investigation looked at the anti-inflammatory effect of BiP on inflamed human synovial tissue transplanted into severe combined immunodeficient mice (SCID), a chimaeric in vivo model previously used to test the efficacy of biologic therapies. Rheumatoid arthritis synovial membrane (RASM) was engrafted into SCID mice. Following successful engraftment, mice were intravenously injected with BiP or human serum albumin in the presence or absence of anti-IL-10 mAb. Twelve days later the grafts were removed for analysis and human cytokines in the sera were quantified by ELISA. The extent of residual inflammatory cellular infiltrate in the synovial explants was determined by weight of the explants. The RASM transplants from mice treated with BiP showed visual reduction in cellular infiltrate and downregulation of all quantifiable features of inflammation as assessed by the Koizumi or Rooney histological criteria. Also downregulated were HLA-DR, CD86, IL-6 and TNFα expression as assessed by immunohistology. ELISA detected significantly less human IL-6 circulating in the BiP-treated mouse serum. After removal of transplanted tissue 12 days post administration of BiP, the RASM explants from the BiP-treated SCID mice weighed significantly less, indicating a suppression of tissue inflammation. Mice given concomitant neutralising anti-IL-10 antibody and BiP showed no such suppression. BiP has anti-inflammatory properties partially dependent on the downregulation of HLA-DR and co-stimulatory molecules and the predominant production of IL-10.
    Arthritis research & therapy 09/2011; 13(5):R149. DOI:10.1186/ar3463 · 3.75 Impact Factor
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    F Ingegnoli · M Blades · A Manzo · S Wahid · M Perretti · G Panayi · C Pitzalis ·
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    ABSTRACT: Adhesion mechanisms play a central role in the recruitment of leukocytes which characteristically infiltrate rheumatoid synovium. Therefore, we adapted an animal model, in which human rheumatoid synovium was transplanted into severe combined immunodeficient (SCID) mice, to study the effects of Tumor Necrosis Factor-alpha (TNF-alpha) in modulatine leukocyte migration and to investigate the chemotactic potential of Stromal Derived Factor-1 alpha (SDF-1 alpha). Human synovium samples, obtained from patients undergoing joint replacement, were divided into two parts. One was analysed by immunohistology and the other was implanted subcutaneously into SCID mice under general anaesthesia. Four weeks post-transplantation, grafts were injected with optimal dose of SDF-1, TNF-alpha or saline (negative control). At the same time, animals were injected iv with fluorescently labelled cells. 48 hours later mice were sacrificed and grafts removed for cryo-hystology. The number of cells migrating to the grafts was determined by UV-microscopy and the results expressed as cells per high power field. In these studies we provide the evidence that: 1) the animal model, in which human tissues are grafted into SCID mice, can be used to study cell migration under controlled experimental conditions; 2) direct intragraft injection of TNF-alpha increases lymphocytes migration and up-regulates the expression of human adhesion molecules (CAMs) and 3) SDF-1 alphainjected intragraft increases the migration of the pro-myelo-monocytic U937 cells to synovial transplants, even more efficiently than TNF-alpha, but without modifications of CAMs' expression.
    Reumatismo 09/2011; 54(2):128-32. DOI:10.4081/reumatismo.2002.128
  • Gabriel S. Panayi · Valerie M. Corrigall ·
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    ABSTRACT: In this chapter we shall review the possible role of heat shock proteins (HSP) and chaperones in the pathogenesis of rheumatoid arthritis (RA). Although HSP/chapcrones are found in all cells, their expression is increased at times of cellular or tissue stress. It is under these conditions that new roles or functions for these proteins will become apparent. Hence, the first section of the review deals with the expression of HSP in the RA synovial membrane (SM). There then follow two sections dealing with the immune response to HSP by patients with RA. The first part considers the antibody responses and the second part the response at the T-cell level. In the third section, we consider the proposal by Roudier and his colleagues that bacterial HSP are involved in the pathogenesis of RA because of molecular mimicry with the shared epitope. This is an innovative concept worthy of separate discussion not least because it is being tested in the clinic. Finally, we review our work on BiP, the endoplasmic reticulum chaperone, which focuses on the concept that HSP/chapcrones may have immunomodulatory or anti-inflammatory effects when found extra-cellularly rather than solely being involved in pro-inflammatory events, which has been the prevailing view to date.
    06/2011: pages 109-137;
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    A M Shields · G S Panayi · V M Corrigall ·
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    ABSTRACT: The resolution of inflammation is central to the maintenance of good health and immune homeostasis. Recently, several intracellular stress proteins have been described as having extracellular properties that are anti-inflammatory or favour the resolution of inflammation. We propose that these molecules should be defined as resolution-associated molecular patterns (RAMPs). RAMPs are released at times of cellular stress and help to counterbalance the inflammatory effects of pathogen-associated (PAMPs) and damage-associated (DAMPs) molecular patterns. We propose that heat shock protein 10 (HSP10), αB-crystallin (αBC), HSP27 and binding immunoglobulin protein (BiP) should be considered founding members of the RAMP family. A greater understanding of RAMP biology may herald the development of novel immunotherapies.
    Clinical & Experimental Immunology 06/2011; 165(3):292-300. DOI:10.1111/j.1365-2249.2011.04433.x · 3.04 Impact Factor
  • Gabriel S Panayi ·

    Rheumatology (Oxford, England) 05/2011; 50(5):815-7. DOI:10.1093/rheumatology/ker024 · 4.48 Impact Factor

  • Annual Meeting of the British-Society-Rheumatology/Spring Meeting of; 04/2010

  • Annals of the Rheumatic Diseases 03/2010; 69(2). DOI:10.1136/ard.2010.129643u · 10.38 Impact Factor
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    Annals of the Rheumatic Diseases 03/2010; 69(2). DOI:10.1136/ard.2010.129593o · 10.38 Impact Factor
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    Gabriel S Panayi ·

    Arthritis & Rheumatology 12/2009; 60(12):3857; author reply 3857-8. DOI:10.1002/art.24997 · 7.76 Impact Factor
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    Alyssa M Macedo · Stephen P Oakley · Gabriel S Panayi · Bruce W Kirkham ·
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    ABSTRACT: Work disability is a serious consequence of rheumatoid arthritis (RA). We conducted a 6-month, prospective randomized controlled trial comparing assessments of function, work, coping, and disease activity in employed patients with RA receiving occupational therapy intervention versus usual care. Employed patients with RA with increased perceived work disability risk were identified by the RA Work Instability Scale (WIS; score >or=10). Patients were stratified into medium- (score >or=10 and <17) and high-risk (>or=17) groups, then randomized into occupational therapy or usual care groups. Assessments were conducted at baseline and 6 months. The primary outcome was the Canadian Occupational Performance Measure (COPM), a standardized patient self-report of function. Other outcomes included the disability index (DI) of the Health Assessment Questionnaire (HAQ); Disease Activity Score in 28 joints (DAS28); RA WIS; EuroQol Index; visual analog scales (VAS) for pain, work satisfaction, and work performance; and days missed/month. Independent sample t-tests and Mann-Whitney U tests were used. We recruited 32 employed patients with RA. At baseline the groups were well matched. At 6 months the improvement in the occupational therapy group was significantly greater than that in the usual care group for all functional outcomes (COPM performance P < 0.001, COPM satisfaction P < 0.001, HAQ DI P = 0.02) and most work outcomes (RA WIS [P = 0.04], VAS work satisfaction [P < 0.001], VAS work performance [P = 0.01]). Additionally, Arthritis Helplessness Index (P = 0.02), Arthritis Impact Measurement Scales II pain subscale (P = 0.03), VAS pain (P = 0.007), EuroQol Index (P = 0.02), EuroQol global (P = 0.02), and DAS28 (P = 0.03) scores significantly improved. Targeted, comprehensive occupational therapy intervention improves functional and work-related outcomes in employed RA patients at risk of work disability.
    Arthritis & Rheumatology 11/2009; 61(11):1522-30. DOI:10.1002/art.24563 · 7.76 Impact Factor
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    Valerie M Corrigall · Olivier Vittecoq · Gabriel S Panayi ·
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    ABSTRACT: Binding immunoglobulin protein (BiP) has been shown previously to have immunomodulatory functions. Herein we investigated whether BiP could affect the differentiation of monocytes into dendritic cells (DCs) and thence the development of regulatory T cells. Peripheral blood monocyte-derived DCs were matured with lipopolysaccharide in the presence or absence of BiP. DC development and T-cell changes were monitored by flow cytometry and regulatory T-cell function was measured by uptake of tritiated thymidine. More BiP-treated DCs (DC((BiP))s) expressed amounts of intracellular indoleamine 2,3-dioxygenase (IDO) and cell surface leucocyte immunoglobulin-like receptor subfamily B member 1 (LILRB1), retained CD14 expression but down-regulated expression of human leucocyte antigen (HLA)-DR and CD86, and produced copious amounts of interleukin (IL)-10, when compared with control DCs. T cells co-cultured with DC((BiP))s developed regulatory function with increased surface expression of CD4(+) CD25(hi) CD27(hi) but with no concomitant increase in forkhead box P3 (Foxp3). These T cells also showed significantly higher levels of intracellular cytotoxic T-lymphocyte antigen (CTLA)-4. The latter could be inhibited by the presence of the IDO inhibitor 1 methyl tryptophan. The addition of neutralizing anti-IL-10 antibody or the specific mitogen-activated protein kinase (MAPK) p38 inhibitor SB203580 reversed the inhibition of DC differentiation by BiP. In conclusion, BiP is an immunomodulator able to arrest inflammation through induction of tolerogenic DCs and subsequent generation of T regulatory cells.
    Immunology 11/2009; 128(2):218-26. DOI:10.1111/j.1365-2567.2009.03103.x · 3.80 Impact Factor
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    ABSTRACT: Patients with rheumatoid arthritis (RA) have increased cardiovascular mortality. Tumour necrosis factor alpha (TNFalpha)-blocking therapy has been shown to reduce RA disease activity measures and joint damage progression. Some observational studies suggest that TNFalpha blockade reduces mortality and incidence of first cardiovascular events. The mechanisms contributing to these outcomes are unclear. This study assessed the effects of infliximab treatment on vascular stiffness and structure in patients with RA. A post hoc analysis of longitudinal data from a randomised placebo controlled study evaluated the effect of infliximab on vascular assessments. 26 patients received intravenous infliximab (3 mg/kg) at weeks 0, 2, 6 and every 8 weeks thereafter to week 54. Patients were followed up to 56 weeks of infliximab therapy with assessments of RA disease activity, cardiovascular risk factors, vascular stiffness (pulse wave velocity (PWV)), carotid intima media thickness (CIMT) and carotid artery plaque (CAP). Univariate analyses of changes over time by repeated measures analysis of variance (ANOVA) were followed by multivariate time-series regression analysis (TSRA) if changes were seen. PWV was significantly lower (better) after 56 weeks of treatment with infliximab (ANOVA p<0.01, TSRA p<0.01). However, CIMT (ANOVA p = 0.50) and CAP (chi(2) = 4.13, p = 0.88) did not change over the study period. Multiple cardiovascular risk measures did not change with treatment and did not correlate with changes in measures of vascular structure. Arterial stiffness improves with infliximab treatment in RA. This change may help explain the improved cardiovascular disease survival in patients with RA receiving TNFalpha-blocking therapy.
    Annals of the rheumatic diseases 10/2008; 68(8):1277-84. DOI:10.1136/ard.2007.086157 · 10.38 Impact Factor

Publication Stats

13k Citations
1,971.18 Total Impact Points


  • 2000-2014
    • King's College London
      • • Department of Academic Rheumatology
      • • Centre for Molecular and Cellular Biology of Inflammation
      • • Florence Nightingale School of Nursing and Midwifery
      Londinium, England, United Kingdom
    • King's College
      Wilkes Barre, Pennsylvania, United States
    • Aristotle University of Thessaloniki
      Saloníki, Central Macedonia, Greece
    • The King's College
      Charlotte, North Carolina, United States
  • 2012
    • Guy's and St Thomas' NHS Foundation Trust
      Londinium, England, United Kingdom
  • 2011
    • University of Milan
      Milano, Lombardy, Italy
  • 2009-2011
    • ICL
      Londinium, England, United Kingdom
  • 2003
    • University College London
      • Department of Internal Medicine
      Londinium, England, United Kingdom
  • 2002
    • WWF United Kingdom
      Londinium, England, United Kingdom
  • 2001
    • Toyama Medical and Pharmaceutical University
      Тояма, Toyama, Japan
  • 1993-1994
    • Northwestern University
      • • Division of Hospital Medicine
      • • Division of Rheumatology
      Evanston, Illinois, United States
  • 1989-1993
    • University of London
      Londinium, England, United Kingdom
  • 1992
    • University of Leuven
      Louvain, Flanders, Belgium
    • University of Ioannina
      • Division of Internal Medicine II
      Ioánnina, Ipeiros, Greece
  • 1984-1990
    • London School of Hygiene and Tropical Medicine
      Londinium, England, United Kingdom
  • 1986
    • Royal Free London NHS Foundation Trust
      Londinium, England, United Kingdom
  • 1983
    • Ashford and St. Peter’s Hospitals NHS Trust
      Chertsey, England, United Kingdom
  • 1980
    • Imperial College Healthcare NHS Trust
      Londinium, England, United Kingdom
    • Arthritis Research UK
      Chesterfield, England, United Kingdom
    • Middlesex Hospital
      मिडलटाउन, Connecticut, United States