| Background:Multiple sclerosis (MS) is currently considered to be an inflammatory disease of the central nervous system (CNS) characterized by focal areas of demyelination in the CNS, also is a myelin antigen-specific T-cell-mediated autoimmune disease. Worldwide, approximately 1,100,000 individuals are afflicted with MS. Women with the disease outnumber men two to one. The etiology is unknown. Genetic factors are important in the development of MS. Contributing environmental determinants (possibly including infectious agents) appear important but remain unidentified. Genome-wide studies have revealed that susceptibility to MS is linked to genes in the major histocompati bility complex (MHC) on chromosome 6. Alleles for certain class n genes, HLA-DR and HLA-DQ, confer the strongest risk of contracting MS. Both cell-mediated and humorally mediated immune mechanisms contribute to pathological injury. The pathogenesis of MS is thought to involve a T-cell-mediated autoimmune process. Axonal damage occurs in addition to demyelization and may be the cause of later permanent disability.Myelin basic protein (MBP) occupy 30% of myelin protein, is a candidate autoantigen in MS because it can induce an MS-like disease, experimental autoimmune encephalomyelitis (EAE), in rodents and primates with susceptible genetic backgrounds. The epitope MBP (85-99), which consists of amino acids 85-99 of MBP, is immunodominant in DR2-positive MS patients and binds to both DRB 1*1501 and DRB5*0101 molecules, though in different registers. The disease relevance of the DRB1*1501-MBP (85-99) complex is supported by data showing that transgenic mice expressing the human DRB 1*1501 molecule and an MS patient-derived TCR that recognizes the DRB1*1501-MBP (85-99) complex develop MS-likedisease. In addition, an antibody that specifically recognizes the DRB 1*1501-MBP (85-99) complex has been used to show that DRB1*1501-MBP (85-99) complexes are present in human MS lesions .The study of pathology found that there were T cells invasion, macrophages invasion and focal areas of demyelization in white matter focus in MS .Grey matter was impinged also. Not only myelin losing,but also neurons denaturation in grey matter and white matter. Traditional theory suggested neurons denaturation is caused by myelin losing, but the study showed there were mass CD44^ CD8-H cells deposition in CSF and MS lesions of CNS, whether MBP specific lymphocytes direct injury neurons,no research confirm.Objectives:There are many research for autoreactive T cells in the autoimmunologic processes of MS, but it is short of the morphological study, especially deficiency the study on neurons.The present study major goal is to observe whether MBP specific lymphycytes directly act on neurons of human brain and myelin sheath. If it is true,we identificat which of the CD4+^ CD8+ cells and NK cells cause obviously impaired effect. Detecting the cell sorting distinction of T lymphocyte subpopulations between affecting neuron and affecting myelin. so as to better explore the mechanism of cytology in MS.Methods:The human MBP 83-99 peptides were synthesized; MTT method was completed to determinate lymphocyte transformation efficiency of MBP synthesitic peptide,and definited suitable acting density of MBP synthesitic peptide; we used flow cytometer(FCM) detect MBP induced T lymphocyte subpopulations; lymphocytes were induced and cultured with MBP synthesitic peptide, subsequently, the induced lymphocytes and nervous cells are co-cultured, observing with scanning electron microscopy (SEM).So as to definite whether or not the neurons of human brain and myelin sheath of axon were aggregated, adhered and attacked by the MBP specific lymphocytes, whether or not neurons and myelin are injuried. Cell marker straining withCD molecular fluorescence-conjugated monoclonal antibodies to identificat T lymphocyte subsets which acting on neuron and myelin ,in order to identificat which of the CD4+, CD8+ ceDs and NK cells cause obviously impaired effect.Results:MB...
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