ArticleClinical and experimental medicine2026
Increased group 2 Innate lymphoid cell (ILC2) activity in pediatric familial mediterranean fever patients with spondyloarthropathy.
Article in Clinical and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Familial Mediterranean fever (FMF), an autoinflammatory disease caused by MEFV mutations, frequently coexists with immune-mediated conditions such as spondyloarthritis (SpA). However, the contribution of innate lymphoid cells (ILCs) to FMF-associated SpA remains poorly defined. Our objective was to characterize the phenotype and functional activity of ILCs in pediatric patients with FMF, SpA, and overlap FMF/SpA. Peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) from FMF (n = 15), SpA (n = 11), FMF/SpA (n = 13), and age-matched healthy controls (n = 14) were analyzed by flow cytometry to quantify ILC subsets. Plasma and synovial cytokines were measured by ELISA, and expression of ILC-associated cytokines in PBMCs and sorted ILCs was assessed by quantitative PCR. Total ILC frequencies and subset distributions in PBMCs and SFMCs were comparable across groups (p > 0.05). However, FMF/SpA patients demonstrated increased IL4 and IL5 expression in sorted ILCs (p < 0.05), consistent with a type 2-skewed ILC activation profile. PBMC thymic stromal lymphopoietin (TSLP) expression was elevated in SpA (p < 0.01). Plasma IL-6, IL-8 and IP-10 concentrations were higher in the full cohort of FMF/SpA patients; however, these differences were sensitive to outlier exclusion and indicate substantial inter-individual heterogeneity. Synovial fluid from SpA patients showed higher IP-10 and IL-17 levels (p < 0.05). Pediatric FMF/SpA is characterized by altered ILC functional polarization rather than numerical expansion, with a prominent type 2 ILC signature. In contrast, SpA displays synovial IP-10 and IL-17 enrichment and increased PBMC TSLP expression. These findings suggest distinct innate immune activation axes in overlap versus isolated SpA and support further investigation of ILC-mediated pathways in FMF-associated spondyloarthritis in larger cohorts.
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