scholarly journals Fine specificity of the antibody response to myelin basic protein in the central nervous system in multiple sclerosis: the minimal B-cell epitope and a model of its features.

1995 ◽  
Vol 92 (24) ◽  
pp. 11061-11065 ◽  
Author(s):  
K. G. Warren ◽  
I. Catz ◽  
L. Steinman
2021 ◽  
Author(s):  
Maryam Sahlolbei ◽  
Maryam Hajizadeh ◽  
Marzie Naseri ◽  
Hossein Ghanbarian ◽  
Seyed Mahmoud Hashemi ◽  
...  

Abstract Over the years, regarding great progresses in knowledge of immunology and neuroscience, the treatment of multiple sclerosis (MS) has been changed. The earlier strategies were focused mainly on T lymphocytes as pioneer cells responsible to inflammatory damage in the central nervous system lesions, whereas B cells, plasma cells and antibodies are also found in the active nerve lesions in MS patients. Despite the accumulating evidence, the role of Myelin basic protein (MBP) antibodies in progression of lesions in nervous system is not completely clear yet. In this regard, here, we present data on B cells and antibody level after MBP immunization of MS mice model. Recombinant fusion protein harboring Myelin basic protein peptide (amino acids 83–99) and CFP was produced in E. coli and purified with chromatography. Then, the C57BL / 6 mice were immunized by rMBP-CFP. Antibody-based assay was used to quantify the level of reactivity to the MBP in mice serum. Subsequently, humoral immunity was analyzed by immunohistochemistry (IHC), ELISA, and Flow cytometry. Our data indicated an increase in autoreactive B cells and MBP specific antibodies after immunization. IHC analysis revealed an increasing penetration rate of immune cells and the nerve lesions development in the nervous system following increasing in MBP antibody titers.This study represented data to support this idea that reactive B cells and antibodies to MBP may contribute to MS pathogenesis. Hence, targeting of these autoreactive B cells and antibodies can be used as potential tools in treatment of MS patients.


1976 ◽  
Vol 156 (3) ◽  
pp. 627-633 ◽  
Author(s):  
G F Buletza ◽  
M E Smith

Proteolytic activity of central-nervous-system tissue of the normal rat was examined over the pH range 2-9 with casein, haemoglobin and myelin basic protein as substrates. With casein as a substrate, brain and spinal cord homogenates showed very similar activity profiles with increasing pH, with the main peaks of proteolytic activity at pH 3-4 and 5-6. When haemoglobin was used, one broad main peak of activity from pH 3 to 5 was demonstrated. There was no optimum pH, however, for proteolytic activity with myelin basic protein as a substrate, and considerable hydrolysis were observed from pH 3.5 up to pH8. Proteolytic activity at the various pH values was compared by using homogenates of spinal cords from rats with acute experimental allergic encephalomyelitis and those from rats injected with Freund's adjuvant alone. The profiles of activity were similar with peaks at pH 3.5 and 5.5 with casein as a substrate, but the specific activity was significantly higher at most pH values in the spinal-cord homogenates from rats with experimental allergic encephalomyelitis. Similarly the spinal-cord homogenates from these latter rats contained much more proteolytic activity toward myelin basic protein throughout the pH range than was present in the control spinal cords. Homogenates from lymph nodes of rats with experimental allergic encephalomyelitis and from those of the controls contained two to three times as much proteolytic activity as that of the central-nervous-system tissue and had a different proteolytic activity profile form that of the central-nervous system, with higher activity at the neutral than at acid pH. The results are discussed with regard to the probability that inflammatory cells such as lymphocytes may be the cause of the increased proteolytic activity in the central nervous system of animals with experimental allergic encephalomyelitis, and that enzymes from these cells possess the capability of digesting myelin basic protein.


1995 ◽  
Vol 182 (2) ◽  
pp. 587-592 ◽  
Author(s):  
S Abromson-Leeman ◽  
R Bronson ◽  
M E Dorf

In vivo adoptive transfer of CD4+ T helper cell type 1 clones reactive with autologous myelin basic protein (MBP) may initiate an inflammatory demyelinating disease of the central nervous system called experimental autoimmune encephalomyelitis. Although MBP is also a component of peripheral nervous system (PNS) myelin, previous studies have failed to demonstrate inflammation in the PNS induced by MBP-reactive T cells. Here, we report on two MBP-specific T cell clones that preferentially initiate inflammatory and demyelinating peripheral neuritis when adoptively transferred to syngeneic recipients. The MBP epitope recognized by these clones spans the junction of exons 6 and 7 and, therefore, is present in the 21- and 18.5-kD but not the 14- and 17-kD MBP isoforms, in which exon 5 is spliced to exon 7. The data suggest that MBP may be processed and presented differently in the central nervous system and PNS, and they provide evidence for MBP as a potential target for autoimmune reactions in the PNS.


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