Biomarkers in Multiple Sclerosis: Analysis of the Present Advantages and Look to the Future

Abstract

MS is a chronic heterogeneous demyelinating disease of the CNS among the young population, manifested by unpredictable attacks and subsequent remissions (McGinley et al., 2021; Lublin et al., 2022). The disease develops as a result of an interaction between genetic and environmental factors (Dobson et al., 2019). The most important genetic risk factor are the alleles of genes encoding human leucocyte antigens (HLAs), especially HLA-DRB1*1501 (Hollenbach et al., 2015). The main exogenous noxes that have the potential to trigger the illness are Epstein Barr Virus (EBV) infection, tobacco use, obesity since childhood, low vitamin D levels. Inflammatory infiltrates within the brain lesions contain CD4 and CD8 T-lymphocytes, activated monocytes and B-lymphocytes which lead to disruption of the myelin sheaths covering the nerves (Housley et al., 2015). It is considered that EBV infection contributes to production of B cells that provokes the activation of CNS inflammatory processes (Leffler et al., 2022). A relationship between gut microbiome-derived short-chain fatty acids (SCFAs) and immune dysfunction in patients with early MS was proposed (Trend et al., 2021). According to a recent hypothesis the EBV infection and B-cell dysfunction connect with gut-associated lymphoid tissue leading to aberrant B-cell responses that guide pathogenic T-cell responses in the CNS (Leffler et al., 2022).