Residual immune activation in cidp remission: the contribution of macrophage-derived cytokines and chemokines.

introductionChronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an immune-mediated neuropathy in which remission does not necessarily imply immunological silence. Persistent low-grade inflammation may continue despite clinical stability. This study aimed to evaluate macrophage-related cytokines and chemokines in CIDP patients during remission compared with healthy controls.

methodsWe conducted a cross-sectional, case-control study including 30 patients fulfilling the 2021 EAN/PNS diagnostic criteria for CIDP in remission and 30 age- and sex-matched healthy controls. All patients received maintenance intravenous immunoglobulin (IVIg). Clinical status was assessed by INCAT scores, and peripheral blood was collected at least one month after the last IVIg infusion. Serum levels of IL-1β, TNF-α, IL-6, MIP-1α, and MIP-1β were measured by ELISA.

resultsCIDP patients had significantly higher IL-1β (p < 0.001) and TNF-α (p = 0.002) levels than controls, whereas IL-6, MIP-1α, and MIP-1β did not differ significantly. IL-1β positively correlated with TNF-α and MIP-1α, suggesting a coordinated inflammatory response. ROC analysis demonstrated moderate diagnostic performance for IL-1β (AUC = 0.783) and TNF-α (AUC = 0.733). No association was observed between biomarker levels and electrophysiological parameters.

conclusionOur findings indicate that residual immune activation persists during CIDP remission, with IL-1β and TNF-α emerging as potential biomarkers of subclinical inflammation. Although MIP-1α and MIP-1β were not elevated in remission, their correlation with proinflammatory cytokines suggests that they may be more relevant in the active phase of disease. Longitudinal studies comparing relapse and remission are warranted to clarify their sensitivity as markers of disease activity and to validate their prognostic role.