Exploring the Association Between IKBKB And IKBKG Protein Levels and the Occurrence of Relapsing-Remitting Multiple Sclerosis

Multiple sclerosis (MS) is a chronic immune-mediated inflammatory disorder that targets and degenerates myelinated neurons within the central nervous system (CNS), ultimately resulting in nontraumatic neurological disability. Approximately 80% of individuals diagnosed with MS exhibit the relapsing-remitting form (RRMS). The etiology of MS is attributed to a sustained disruption of immune homeostasis arising from intricate interactions between genetic predisposition and environmental determinants. The IKK2 (IKBKB) acts as a key mediator in activating the nuclear factor kappa-lightchain-enhancer of activated B cells (NF-κB) signaling pathway. This activation boosts NF-κB signaling activity, leading to functional dysregulation in both T and B lymphocytes. Likewise, the NEMO/IKKγ (IKBKG) is essential for activating the NF-κB pathway and is involved in a wide range of physiological and cellular processes, including immune regulation, inflammatory response, cell proliferation, and survival. The NF-κB signaling pathway has been extensively linked to the development of numerous human disorders, especially those marked by chronic inflammation. This study aimed to determine the associations between IKBKB and IKBKG protein concentrations and the occurrence of relapsing-remitting multiple sclerosis. The concentrations of IKBKB and IKBKG proteins in blood serum were determined using the enzyme-linked immunosorbent assay (ELISA) method. Statistical data analysis was performed using SPSS software. It was found that IKBKB serum concentration was statistically significantly higher in RRMS patients compared with the control group (median (IQR): 1.78 (1.44) vs. 1.37 (0.81), p = 0.002). IKBKB analysis showed no statistically significant differences between RRMS patients and control groups (median (IQR): 0.21 (0.14) vs. 0.17 (0.10), p=0.110). The study demonstrated that serum IKBKB concentration was significantly elevated in RRMS patients compared with healthy controls, suggesting a potential involvement of IKBKB in disease mechanisms. In contrast, IKBKG levels showed no statistically significant differences between the groups.