Basic information of Mbp :
| Official Symbol of Gene | Mbp |
| Species | Mus musculus |
| Entrez Gene ID | 17196 |
| Official Full Name | myelin basic protein |
| Also known as | jve; mld; shi; Hmbpr; golli-mbp |
| Gene Type | protein coding |
| dbXrefs | Ensembl:ENSMUSG00000041607 AllianceGenome:MGI:96925 |
| Map Location | 18 E3; 18 55.84 cM |
Sample information of multiple sclerosis:
| Detected Sample | Peripheral blood |
| Sample Detail | N/A |
| Detected Method | ELISA |
| Disease | EAE |
| Disease subtype | N/A |
| Population | Female SJL/J mice |
| Sample Size | n = 5–6 mice group |
Literature information of multiple sclerosis :
| Pubmed ID | 10466625 |
| Year | 1999 |
| Title | Prevention of Experimental Allergic Encephalomyelitis by Intramuscular Gene Transfer with Cytokine-Encoding Plasmid Vectors |
Results of multiple sclerosis :
| Expression | up-regulation |
| Risk type | Disease risk |
| Result | TGF-b1 gene delivery had pronounced downregulatory effects on T cell proliferation and production of interferon c (IFN-c ) and tumor necrosis factor a (TNF-a), on in vitro restimulation with MBP. IL-4-IgG1 vector administration also suppressed these responses, although much less than TGF-b1, and enhanced secretion of endogenous IL-4. Therapy resulted in a significant decrease in the severity of histopathologic inflammatory lesions. In the CNS, treatment with either vector suppressed IL-12 and IFN-c mRNA expression, while IL-4 and TGF-b1 mRNA levels were increased compared with control mice. Thus, cytokine plasmid treatment appeared to inhibit MBP-specific pathogenic Th1 responses, while enhancing endogenous secretion of protective cytokines. We demonstrate that gene therapy with these vectors is an effective therapeutic strategy for EAE |
| Mechanism/Pathway | We studied the immunoregulatory properties of TGF-b1 and IL-4 in an animal model of EAE, by direct intramusculas injection of plasmid DNA expression vectors encoding either TGF-b1 (pVR-TGF-b1) or an IL-4–IgG1 chimeric protein (pVR-IL-4-IgG1). Treatment with either vector resulted in cytokine production capable of suppressing CNS inflammation in mice with MBP-induced EAE. Both cytokines had downregulatory effects on T cell proliferation, and production of proinflammatory cytokines, although TGF-b1 was more suppressive. As well, cytokine gene therapy enhanced the production of endogenous regulatory cytokines in lymph node cells and CNS tissue. Somatic cytokine gene therapy proved to be effective in this autoim- mune disease. |
