POS0440 INCREASED FREQUENCY OF ACTIVATED MAIT CELLS EXPRESSING THE GUT HOMING RECEPTOR CCR9 IN PATIENTS WITH RADIOGRAPHIC AXIAL SPONDYLOARTHRITIS

• Published in: Annals of the rheumatic diseases Vol. 82; no. Suppl 1; pp. 475 - 476
• Main Authors: Toussirot, E., Laheurte, C., Gravelin, E., Vauchy, C., Puyraveau, M., Saas, P.
• Format: Journal Article
• Language: English
• Published: Kidlington BMJ Publishing Group Ltd and European League Against Rheumatism 01.06.2023; Elsevier B.V; Elsevier Limited
• Subjects: Age; Ankylosing spondylitis; Arthritis; CC chemokine receptors; CD3 antigen; CD4 antigen; CD49d antigen; CD69 antigen; CD8 antigen; Chemokine receptors; Chemokines; Dipeptidyl-peptidase IV; Flow cytometry; Gastrointestinal tract; Homing receptors; Inflammatory diseases; Innate immunity; Interleukin 17; Interleukin 22; Lymphocytes T; Mucosa; Nonsteroidal anti-inflammatory drugs; Peripheral blood; Rheumatic diseases; Scientific Abstracts; Spondyloarthritis; T cell receptors; γ-Interferon; Innate immunity; Spondyloarthritis; Gastrointestinal tract
• ISSN: 0003-4967; 1468-2060
• DOI: 10.1136/annrheumdis-2023-eular.2383

BackgroundMAIT (mucosal associated invariant T) cells are involved in mucosa defense against bacteria. This cellular subset is characterized by a semi-invariant αβ TCR and the expression of CD161. In patients with axial spondyloarthritis (ax SpA), previous works reported a decreased frequency of circulating MAIT cells compared to normal subjects. IL-17A is a relevant cytokine involved in SpA pathophysiology. MAIT cells are a cellular source of IL-17 and IL-17+ MAIT cells were found increased in ax SpA. We have previously reported an increased frequency of IFNγ+/IL-17+ MAIT cells as well as IL-22+ MAIT cells in ax SpA[1].ObjectivesIn this study, we aimed to complete our previous results by evaluating activation markers and chemokine receptor/integrin expression, especially those for gut homing, in MAIT cells.Methodspatients exhibited ax SpA (ASAS criteria) with a radiographic (r-ax SpA) or non-radiographic (nr-ax SpA) form. They all were under NSAIDs and biologic naïve. Healthy subjects were recruited as controls (HC). Circulating CD4+ and CD8+ T cells and MAIT cells were determined on blood samples by single platform flow cytometry (Cytoflex, Beckman Coulter). MAIT cells were identified by the co-expression of CD3, CD161 and TCRα7.2. In each subpopulation, we examined the expression of CD26, CD69, CCR9 and CD49d integrin.Results26 patients were included (11 r-ax SpA: 9 males [M]; mean age 54.1 ± 19.6 years; disease duration: 16.2 years; ASDAS score: 4.1; and 15 nr-ax SpA: 7 M; age: 36.4 ± 1.3; ASDAS: 5.6) and 27 HC (16 M; age: 43 ± 12.7). In patients with r-ax SpA, we observed an increased frequency of activated CD3+ CD69+ MAIT cells and CD3+ MAIT cells expressing the gut homing markers CCR9 and CD49d, as compared to HC (p <0.05). These higher frequencies were not observed in patients with nr-ax SpA. In addition, when examining the CD8+ MAIT population, similar higher frequencies of cells positive for CD69, CCR9 and CD49d were observed in patients with r-ax SpA compared to HC and patients with nr-ax SpA (p<0.01 and p<0.05, respectively).These modifications were specific for MAIT cells and were not observed in conventional CD4+ or CD8+ T lymphocytes.Table.HCr-ax SpAnr-ax SpA% CD69+ MAIT CD3+18.4 ± 9.928.3 ± 14.7 *19.7 ± 10.3% CD69+ MAIT CD8+19.1 ± 11.429.5 ± 15.6 *20.8 ± 12.0% CD49d+CCR9+ MAIT CD3+1.6 ± 1.72.5 ± 1.6 *1.9 ± 2.3% CD49d+CCR9+ MAIT CD8+1.4 ± 1.72.5 ± 1.8**1.7 ± 2ConclusionPatients with r-ax SpA are characterized by an increased frequency of activated MAIT cells that expressed homing receptors (chemokine and integrin) for the gut. These results confirm that MAIT cells are altered in ax SpA and highlight the relationships between ax SpA and gut inflammation, especially for the radiographic form.Figure 1.Reference[1]Toussirot E, Laheurte C, Gaugler B, Gabriel D, Saas P. Increased IL-22- and IL-17A-producing Mucosal-Associated Invariant T cells in the peripheral blood of patients with ankylosing spondylitis. Front Immunol. 2018; 9:1610.Acknowledgements:NIL.Disclosure of InterestsNone Declared.