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Response to: ‘Potential roles for tenascin in (very) early diagnosis and treatment of rheumatoid arthritis’ by Cutolo et al
  1. Susan Aungier1,
  2. Alison J Cartwright1,
  3. Anja Schwenzer1,
  4. Jennifer Marshall2,
  5. Mike R Dyson3,
  6. Peter Slavny3,
  7. Kothai Parthiban3,
  8. Aneesh Karatt-Vellatt3,
  9. Ilfita Sahbudin4,5,
  10. Eric Culbert6,
  11. Patrick Hextall6,
  12. Felix IL Clanchy1,
  13. Richard Williams1,
  14. Brian D Marsden1,7,
  15. Karim Raza2,8,
  16. Andrew Filer2,
  17. Christopher D Buckley1,2,
  18. John McCafferty3,
  19. Kim S Midwood1
  1. 1 Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK
  2. 2 Institute of Inflammation and Ageing, University of Birmingham, Queen Elizabeth Hospital, Birmingham, UK
  3. 3 IONTAS Ltd, Cambridge, UK
  4. 4 Rheumatology Research Group, School of Immunity and Infection, Birmingham, UK
  5. 5 University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
  6. 6 Nascient, Cambridge, UK
  7. 7 Structural Genomics Consortium, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK
  8. 8 Department of Rheumatology, Sandwell and West Birmingham Hospitals NHS Trust, Birmingham, UK
  1. Correspondence to Professor Kim S Midwood, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Kennedy Institute of Rheumatology, Oxford OX3 7FY, UK; kim.midwood{at}

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We thank the authors for their commentary1 on our article which was recently published in the Annals of Rheumatic Diseases.2 Cutolo et al write an extended discussion of the study, in which we describe the development of therapeutic monoclonal antibodies that block the pro-inflammatory activity of the fibrinogen-like globe (FBG) domain of tenascin-C, and the efficacy of these antibodies in preventing disease progression in preclinical models of rheumatoid arthritis (RA). The commentary includes a detailed summary of the autoantibody response to a citrullinated epitope (cTNC5) within the FBG domain of tenascin-C which arises very early during the development of RA, and which can also be detected in around one in five people at risk of developing RA. As highlighted by the authors, the questions around how the response …

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  • Handling editor Josef S Smolen

  • Contributors All authors reviewed the response.

  • Funding This work was supported by grants from Nascient Ltd (SRA, AJC, FC and JLM), Arthritis Research UK Fellowships (20003: AS and KSM) and (18547: AF),and an Arthritis Research UK programme grant (19791: CDB). This work was also supported by the Arthritis Research UK Rheumatoid Arthritis Pathogenesis Centre of Excellence (20298). BDM was supported by the SGC and by the Kennedy Trust for Rheumatology Research. This report includes independent research supported by the National Institute for Health Research/Wellcome Trust Clinical Research Facility at University Hospitals Birmingham NHS Foundation Trust.

  • Disclaimer The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health. KR, IS, AF and CDB were supported by the National Institutefor Health Research (NIHR) Birmingham Biomedical Research Centre.

  • Competing interests MRD, PS, KP, AK-V and JLM are employed by IONTAS. EC and PH are employed by Nascient. KSM is a founder and director of Nascient Ltd.AF has received research funding from Roche and Pfizer. KR has received research funding from Abbvie and Pfizer and honoraria/consultancy fees from Lilly, BMS,UCB, Pfizer, Janssen and Roche Chugai. JLM is currently funded by Roche Holding AG. BDM was partly supported by the SGC, which is a registered charity (number1097737) that receives funds from AbbVie, Bayer Pharma AG, Boehringer Ingelheim,Canada Foundation for Innovation, Eshelman Institute for Innovation, Genome Canada through Ontario Genomics Institute (OGI-055), Innovative Medicines Initiative (EU/EFPIA) (ULTRA-DD grant no. 115766), Janssen, Merck KGaA, Darmstadt, Germany, MSD, Novartis Pharma AG, Ontario Ministry of Research,Innovation and Science (MRIS), Pfizer, Sao Paulo Research Foundation – FAPESP, Takeda and Wellcome (106169/ZZ14/Z).

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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