Background/Purpose: Innate lymphoid cells (ILCs) produce disease-related cytokines including IL-17 and IL-22 and are therefore of substantial interest in PsA. Spreading the disease from the skin to the joints most likely requires trafficking of cells through the circulation. Upon perturbation of immune homeostasis, the pool of resident ILCs is replenished by migration of ILCs into the peripheral blood. Tackling their potential contribution to immunopathology of PsA we quantified circulating ILC subsets in PsA patients in correlation to disease activity and structural tissue damage.

Methods: 124 patients satisfying the Classification Criteria for Psoriatic Arthritis (CASPAR) and 26 healthy volunteers were enrolled in the study. Information regarding the tender and swollen joint count of 68 joints, the visual analogue scala (VAS) of pain and global assessment, presence of plaque psoriasis, psoriatic nail dystrophy, enthesitis, history of uveitis/iritis, CRP levels, erythrocyte sedimentation rate, imaging results (MRI and high-resolution peripheral quantitative CT) were collected and disease activity score 28 (DAS28), disease activity in psoriatic arthritis (DAPSA), minimal disease activity score (MDA) were calculated. MRI and high-resolution peripheral CT were taken and PsA MRI score (PsAMRIS) was assessed. Flow cytometric analysis was performed and IFNγ-producing ILC1s, IL-4/IL-5-producing ILC2s and IL-17/IL-22-producing ILC3s were identified among ILCs. Multivariate linear regression and Receiver-Operating Characteristic (ROC) Curve analysis was performed using the IBM SPSS Statistics software.

Results: Total number of circulating ILCs were increased in PsA patients compared to healthy controls (p˂0,001). Linear regression analyses of the relationship between disease activity and circulating ILC counts showed that ILC2 negatively (R = -3732; p < 0.0001) and ILC1 and ILC3 positively correlated with DAPSA score (R = 0.2622, p = 0.0057; R = 0.4092, p < 0.0001 respectively). The strongest correlation was observed when the ratio of ILC2 to ILC3 was analyzed (R = -0.5709; p < 0.0001). ILC2/3 ratio was also reduced in patients with active psoriatic skin disease, presence of enthesitis or a history of concomitant uveitis. Extend of synovitis or tenosynovitis or presence of bone erosions or osteophytes on MRI was inversely correlated with the ILC2/3 ratio (R = -0.6753; p < 0.0001, R = -0.5828; p = 0.0011 and p < 0.001 respectively). Consistently, presence of erosions and/or osteoproliferation assessed by HR-pQCT was correlated with a significant lower ILC2/3 ratio. Furthermore, ROC Curve was used to test the performance of the ILC2/3 ratio as marker in differentiating between remission and disease activity of PsA. Indeed, a cut-off 0.57 exhibited highest sensitivity (92.9%) and a 84.7% specificity in identifying remission.

Conclusion: We show that perturbed ILC homeostasis is correlated with both composite clinical disease activity scores and with imaging signs of inflammation and structural damage suggesting pathogenic impact of ILCs in PsA. Further studies are necessary to validate ILC2/ILC3 ratio as biomarker for immunological disease activity in PsA.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/innate-lymphoid-cells-new-players-in-psoriatic-arthritis/