The course of cytokine and chemokine gene expression in clinically suspect arthralgia patients during progression to inflammatory arthritis

Autoantibody responses increase years before the onset of inflammatory arthritis (IA) and are stable during transitioning from clinically suspect arthralgia (CSA) to IA. Cytokine and chemokine levels also increase years before IA onset. However, the course in the at-risk stage of CSA during progress...

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Veröffentlicht in:Rheumatology (Oxford, England) England), 2024-02, Vol.63 (2), p.563-570
Hauptverfasser: Heutz, Judith W, Rogier, Cleo, Niemantsverdriet, Ellis, van den Eeden, Susan J F, de Jong, Pascal H P, Lubberts, Erik, Geluk, Annemieke, van der Helm-van Mil, Annette H M
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Sprache:eng
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Zusammenfassung:Autoantibody responses increase years before the onset of inflammatory arthritis (IA) and are stable during transitioning from clinically suspect arthralgia (CSA) to IA. Cytokine and chemokine levels also increase years before IA onset. However, the course in the at-risk stage of CSA during progression to disease or non-progression is unknown. To increase the understanding of processes mediating disease development, we studied the course of cytokine, chemokine and related receptors gene expression in CSA patients during progression to IA and in CSA patients who ultimately did not develop IA. Whole-blood RNA expression of 37 inflammatory cytokines, chemokines and related receptors was determined by dual-colour reverse transcription multiplex ligation-dependent probe amplification in paired samples of CSA patients at CSA onset and either at IA development or after 24 months without IA development. ACPA-positive and ACPA-negative CSA patients developing IA were compared at CSA onset and during progression to IA. Generalised estimating equations tested changes over time. A false discovery rate approach was applied. None of the cytokine/chemokine genes significantly changed in expression between CSA onset and IA development. In CSA patients without IA development, G-CSF expression decreased (P = 0.001), whereas CCR6 and TNIP1 expression increased (P 
ISSN:1462-0324
1462-0332
1462-0332
DOI:10.1093/rheumatology/kead238