Sherman Maryam Sahlolbei, Maryam Hajizadeh, Marzieh Naseri, Leili Saeednejad Zanjani, Hossein Ghanbarian, Zahra Madjd, Seyed Mahmoud Hashemi, Jafar Kiani
Background: Over the years, the treatment of multiple sclerosis (MS) has improved due to the dramatic advancement in immunology and neuroscience. The recent therapeutic approaches substantially expanded our view of the role of B cells in the progression of MS. The present study aimed to investigate the role of B cells and Myelin Basic Protein (MBP)-induced antibodies in developing Experimental Autoimmune Encephalomyelitis (EAE, an animal model of multiple sclerosis).
Method: We used MBP for induced experimental autoimmune encephalomyelitis in C57BL/6 female mice and analyzed the clinical score. The Enzyme-Linked Immunosorbent Assay (ELISA) and western blot assessed the expression of MBP-induced antibodies. The infiltration rate of the inflammatory cells and demyelination in the spinal cord were also evaluated by Hematoxylin/Eosin, Luxol fast blue, or anti-MBP staining procedures. Besides, the fluorescent Immunohistochemistry (IHC) was used to detect T and B cells infiltration in the spinal cord, and both T and B cells were counted by flow cytometry.
Result: These findings indicated that MBP immunization significantly increased B cells and anti-MBP-antibodies. IHC analysis revealed a significant increase in the penetration rate of immune cells and the development of nerve damage in the spinal cord. Moreover, MBP antibody levels directly correlate with immune cell infiltration in the spinal cord (p < 0.001).
Conclusion: This study supports the idea that reactive B cells and MBP-induced antibodies may contribute to the pathogenesis of EAE. Further studies are needed to investigate targeting B cells and MBP-induced antibodies as potential therapeutic strategies for treating multiple sclerosis.