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Autoimmune Rheumatic Diseases

Comparative Analysis of CXCR5 Circulating DNA Methylation Levels in Autoimmune Rheumatic Diseases


Objective


To assess CXC chemokine receptor 5 (CXCR5) circulating DNA methylation differences in autoimmune rheumatic diseases and their relation with clinical features.

Methods


Targeted methylation sequencing was performed using peripheral blood from 164 rheumatoid arthritis (RA), 30 systemic lupus erythematosus (SLE), 30 ankylosing spondylitis (AS), 30 psoriatic arthritis (PsA), 24 Sjögren's syndrome (SS) patients, and 30 healthy controls (HC).

Results


Significant differences in CXCR5 cg19599951 methylation were found between RA and HC, as well as AS and SLE. RA patients exhibited higher methylation than HC and AS (p < 0.01) but lower than SLE (p < 0.05). SLE patients showed higher methylation compared to HC, AS, and PsA (p < 0.001, 0.01, and 0.05, respectively). No significant differences were found in patients with SS compared to other autoimmune diseases and HC. Methylation at cg19599951_103 (r = 0.17, p < 0.05) and cg19599951_209 (r = 0.22, p < 0.01), along with the CC haplotype (r = 0.21, p < 0.01), showed significant positive correlations with erythrocyte sedimentation rate (ESR), while the CT (r = −0.27, p < 0.001) and TT haplotypes (r = −0.19, p < 0.05) were negatively correlated. For C-reactive protein (CRP), methylation at cg19599951_103 (r = 0.29, p < 0.001) and cg19599951_209 (r = 0.33, p < 0.0001), and the CC haplotype (r = 0.34, p < 0.0001) was positively correlated, whereas the CT (r = −0.36, p < 0.0001) and TT (r = −0.30, p < 0.0001) haplotypes were negatively correlated. Significant negative correlations were observed between the CT haplotype and rheumatoid factor (r = −0.25, p < 0.01), and anti-citrullinated protein antibody (r = −0.20, p < 0.05). No significant correlations were found in patients with SLE, AS, and SS. Receiver operating characteristic analysis showed CXCR5 methylation could classify patients with RA versus those with AS (AUC: 0.624−0.967).

Conclusion


Differential circulating CXCR5 methylation levels were observed in autoimmune rheumatic diseases, which correlated with inflammatory mediators in RA and may serve as potential biomarkers for RA diagnosis.

Our findings revealed significant differences in CXCR5 circulating methylation levels between patients with RA and those with SLE relative to healthy individuals, and notable differences between patients with RA and those with AS and SLE. CXCR5 methylation levels were able to distinctly differentiate patients with CCP-negative RA from those with AS. Additionally, CXCR5 methylation levels in patients with RA were significantly correlated with inflammatory markers. 

The results further substantiated that alterations in CXCR5 methylation have a role in the pathogenesis of autoimmune illnesses and could potentially serve as markers reflecting the inflammatory levels in RA, assisting disease diagnosis. The underlying mechanisms behind these differential methylation patterns warrant further investigation, especially in terms of how CXCR5 methylation specifically influences immune function and disease progression. Subsequent studies may also explore the methylation status of additional inflammation signaling pathways related to ARDs, to clarify the epigenetic regulatory landscape shaping these pathologies.

rheumatoid arthritis, systemic lupus erythematosus, scleroderma, Sjögren's syndrome, polymyositis, dermatomyositis, ankylosing spondylitis, psoriatic arthritis, vasculitis, antiphospholipid syndrome, connective tissue disease, autoantibodies, chronic inflammation, immune dysregulation, joint pain, fatigue, immunosuppressive therapy, biologics, cytokines

#AutoimmuneDiseases, #RheumaticDiseases, #LupusAwareness, #RheumatoidArthritis, #SclerodermaWarrior, #SjogrensSyndrome, #VasculitisAwareness, #PsoriaticArthritis, #ChronicIllness, #Inflammation, #Autoimmunity, #JointPain, #ImmuneSystem, #BiologicTherapy, #ConnectiveTissueDisease, #Fatigue, #Autoantibodies, #ImmuneHealth, #ArthritisSupport, #RAAwareness

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