Abstract
BackgroundMultiple sclerosis is a demyelinating and autoimmune disease and its immune response is not fully elucidated. This study was conducted to examine the pathological changes and B cell subsets in experimental autoimmune encephalomyelitis (EAE) mice, and analyze the expression of triosephosphate isomerase (TPI) and GADPH to define the role of B cell subsets in the disease.ResultsFemale C57BL/6 mice were randomly divided into EAE group (n = 18) and control (n = 18). During the experiments, the weight and nerve function scores were determined. The proportions of B cell subsets in the peripheral blood were measured by flow cytometry. Seven, 18 and 30 days after immunization, the brain and spinal cord tissues were examined for the infiltration of inflammatory cells using hematoxylin-eosin (HE) HE staining and the demyelination using Luxol fast blue staining. The expression of B cell-related proteins was detected immunohistochemistrially and the expression of antigenic TPI and GADPH was analyzed using enzyme-linked immunosorbent assay (ELISA). HE staining showed that mice had more severe EAE 18 d than 7 d after modelling, while the symptoms were significantly relieved at 30 d. The results were consistent with the weight measurements and neural function scores. Immunohistochemistry studies showed that B cells aggregated in the spinal cord, but not much in the brain. Flow cytometry studies showed that there were more B cells in control than in EAE models from day 7 and the difference was narrowed at day 30. The level of plasma cells increased continuously, reached the top at day 21 and obviously declined at day 30. On other hand, the numbers of memory B cells increased gradually over the experimental period. The numbers of plasma and memory B cells were similar between the control and EAE mice. ELISA data revealed that the brain contents of TPI and GAPDH were higher in EAE mice than in control at day 7, while at day 18, the levels were reversed.ConclusionsIn the central pathological process of EAE mice, B cells exert role through the mechanism other than producing antibodies and the levels of brain TPI and GADPH are related to the severity of autoimmune induced-damage.
Highlights
Multiple sclerosis is a demyelinating and autoimmune disease and its immune response is not fully elucidated
Other studies have found that the level of antibody in the plasma cells and cerebrospinal fluid in Multiple sclerosis (MS) patients is basically unchanged after receiving B cell depletion therapy, and B cells may play role in MS via other mechanisms [6]
Changes in B cell subsets Flow cytometry showed that the percentage of activated B cells in peripheral blood decreased from the 7th day, and was significantly lower in EAE group than in control group from the 14th day
Summary
Multiple sclerosis is a demyelinating and autoimmune disease and its immune response is not fully elucidated. Multiple sclerosis (MS) is a demyelinating disease in the white matter of the central nervous system. It is an autoimmune disease associated with genetic and environmental factors in susceptible individuals. A variety of Recent studies have found that during the pathogenesis of MS, B cells play an important role. Other studies have found that the level of antibody in the plasma cells and cerebrospinal fluid in MS patients is basically unchanged after receiving B cell depletion therapy, and B cells may play role in MS via other mechanisms [6]. The antibodies and the single-strand variable fragment antibodies in the cerebrospinal fluid of MS patients were immunoreactive to GAPDH, suggesting that GAPDH could promote the proliferation of B cells in the central nervous system in MS patients [9, 10]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
