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Response to: ‘Correspondence to ‘Normal human enthesis harbours conventional CD4+ and CD8+ T cells with regulatory features and inducible IL-17A and TNF expression’’ by Wang and Ma
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  1. Abdulla Watad1,
  2. Charlie Bridgewood2,
  3. Dennis G McGonagle3
  1. 1Internal medicine, Sheba Medical Center at Tel Hashomer, Tel Hashomer, Israel
  2. 2LIRMM, Leeds, UK
  3. 3Chapel Allerton Hospital, Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, NIHR Leeds Biomedical Research Centre, Leeds, UK
  1. Correspondence to Dr Abdulla Watad, Internal medicine, Sheba Medical Center at Tel Hashomer, Tel Hashomer, Israel; watad.abdulla{at}gmail.com

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We thank Wang and Ma1 for their comments on our description of T-cells and their cytokines profile at the normal human spinal enthesis.2 Wang and Ma1 report on synovial T-cells in psoriatic arthritis (PsA) obtained from synovial biopsies, and amongst other things, describes that infliximab therapy leads to a reduction in interleukin (IL)-23 related pathway transcripts indicating a potential pathogenic interplay between tumour necrosis factor (TNF)-α and IL-23/IL-17 axis at the synovium.1

The enthesis and synovium form what is known as the synovio-entheseal structure complex.3 A major unresolved issue in the immunopathology of PsA, is the link between synovial and entheseal immune cells. Animal models suggest that disease either TNF or IL-23 originating enthesitis may drive synovitis,4 5 but it is unclear if this is the case humans. It is possible that the findings of Wang and Ma1 could be extended to the enthesis and bone but formal studies are needed since the precise link between these immune compartments is unclear. The authors’ results suggest a ‘dampening’ of the IL-23/IL-17 axis following infliximab therapy by acting on TGF-β and aryl hydrocarbon receptor signalling, that are involved in the regulation of the 23/17 axis. These findings are of interest towards the further understanding of the link between the enthesis and synovium in PsA and spondyloarthritis.

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors All the authors have contributed to writing and reviewing the final draft.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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