Whole transcriptomic analysis identified differentially dysregulated immune and neurological pathways in relapse and remission phases of experimental autoimmune encephalomyelitis

Multiple sclerosis (MS) is a neurodegenerative disorder that is characterized by chronic inflammation and demyelination of the central nervous system (CNS). Most affected patients undergo relapse and remission stages. Relapse episodes represent one of the most challenges in the treatment of MS as overtime frequent relapses result in the accumulation of unreversed damage in the CNS. Relapse is correlated with genetic and environmental factors, however, the molecular mechanisms that are associated with it are still unclear. This study aims to investigate the mechanisms of MS relapse and remission using its animal model experimental autoimmune encephalomyelitis (EAE). via transcriptomic analysis was used, and several factors were found to participate in the initiation of the relapse in EAE disease, including dysregulation of signalling pathways such as PI3K/Akt, MAPK, and JAK/STAT pathways. In addition, increased numbers of immune cells such as activated natural killer (NK) cells were observed in relapse. whereas other properties characterize the remission including high percentages of Tregs, B and T CD8+ lymphocytes, and increased expression of prolactin (Prl) hormone. Taken together, dysregulation of these molecular pathways may potentially contribute to decreased inflammation and myelin repair and regeneration in the remission EAE phase