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Letter
Cardiac valve immune profiling in non-radiographic axial spondyloarthritis
  1. Zoya Qaiyum1,
  2. Michael Aaron Seidman2,3,
  3. Heather Joan Ross4,5,
  4. Robert D Inman1,6,7
  1. 1 Schroeder Arthritis Institute, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada
  2. 2 Laboratory Medicine Program, University Health Network, Toronto, Ontario, Canada
  3. 3 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada
  4. 4 Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada
  5. 5 Division of Cardiology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada
  6. 6 Department of Immunology, University of Toronto, Toronto, Ontario, Canada
  7. 7 Department of Medicine, University of Toronto, Toronto, Ontario, Canada
  1. Correspondence to Dr Robert D Inman; robert.inman{at}uhn.ca

https://doi.org/10.1136/ard-2024-225942

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    The diagnosis of ankylosing spondylitis (AS) is anchored in diagnostic changes in the sacroiliac joints as detected by pelvic X-rays.1 Recognising that symptoms could precede radiographic changes, often for prolonged periods of time, the clinical entity of axial spondyloarthritis (axSpA) has been broadened to include non-radiographic axSpA (nr-axSpA) as well as AS.1 Nr-axSpA is usually dependent on MRI evidence of inflammation in the sacroiliac joints.1 Whether nr-axSpA is a distinct entity or part of the spectrum of a single disease has been debated.2 The commonality of extra-articular manifestations has been cited in support of the latter theory.3

    Cardiovascular disease is found in 2%–10% of AS patients and generally manifests as valvular heart disease (VHD), aortitis, cardiomyopathy or ischaemic heart disease.4 Aortic regurgitation (AR) is the most frequently reported VHD in AS.4 There is evidence that suggests the disease duration of axSpA may relate to the development of cardiac manifestations, particularly aortic root and valvular disease.3

    Inflammation in cardiac valves has not been reported in nr-axSpA to date, despite being recognised as a clinical feature of AS. Furthermore, there has been no study of the immunological profile underlying the inflammation in the valve. We previously identified a subpopulation of pathogenic mature CD8+T cells in the AS joint, expressing CD103+ and CD49a+integrins, termed InEx cells.5 Integrins are adhesion molecules which orchestrate the exit of leucocytes from the circulation, resulting in target organ tropism and retention in various tissues.5 In particular, the expression of CD103 and CD49a integrins has been found in gut and skin-resident lymphocytes,6 reminiscent of a resident memory phenotype with cytotoxic capacity.5 6 Here, we report the spatial and immunological profile of the aortic valve (AV) using imaging mass cytometry (IMC), highlighting a role for the integrins CD103 …

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    Footnotes

    • Handling editor Josef S Smolen

    • Contributors ZQ and RDI were involved with study conception and design. Aortic tissue was stained and imaged using imaging mass cytometry at Therapeutic Insights Services (Fluidigm). ZQ analysed and interpreted the resulting raw data. ZQ, MAS, HJR and RDI wrote the manuscript. All authors agreed to publish the data and reviewed the manuscript. RDI serves as the guarantor for the overall content, accepts full responsibility for the finished work and/or the conduct of the study, had access to the data and controlled the decision to publish.

    • Funding This study was supported by the Canadian Institutes of Health Research (CIHR) grant number 410010059.

    • 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.

    • Provenance and peer review Not commissioned; externally peer reviewed.