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BACKGROUND: Multiple sclerosis(MS) is a chronic autoimmune disease induced by the interaction between genetic and environmental factors. Its pathogen and the mechanism of the relapse and remission m the course of the disease are still unknown. Most of the MS research centers are looking for the pathogenic polypeptide epitope in proteolipid protein(PLP), myelin sheath basic protein (MBP) and oligodendrocyte glycoprotein (MOG) OBJECTIVE: To compare the proliferation of T cell lines(TCL) in MS induced by myelin sheath and delipidated myelin sheath towards 11 components of myelin sheath to mainly search the possible pathogenic polypeptide epitope in PLP, and investigate the possible effects of abnormal dcgrease in myelin sheath.DESIGN: A case-controlled trial.SETTING: Department of neurology in a hospital of a university.PARTICIPANTS: Mononuclear cells(MNC) of 16 MS cases(clinical relapsing-remitting type, patients did not receive any immunosuppresant for at least 3 months when their peripheral blood samples were taken) and 12 HLA-DR15 healthy volunteers were furnished by Dr. Trotter JL of MS Research Center of Washington University from the cell database.INTERVENTIONS: MS-TCL and normal TCL were induced twice by stimulation with myelin sheath and delipidated myelin sheath in vitro by cell culture in vitro. TCL proliferation was tested by 11 antigens including PLP,MBP, M87-106, P30-49, P40-60, P89-106, P95-117, P117-137,P139-151, P178-191, and P185-206.MAIN OUTCOME MEASURES: Difference of scintillation counting in every minute of every well, and the stimulative index of each well were calculated, and the mean wells with positive proliferation of TCL towards each antigen were confirmed as well.RESULTS: The general specific proliferation towards myelin sheath antigens was bigger in MS group than control group 5.49 ±5.31 to 3.10 ± 3. 17, and delipidated myelin sheath-induced TCL was bigger than myelin sheath-induced one 5. 49 ± 5.31 to 3.41 ± 4. 83 . Delipidated myelin sheath significantly changed the immune responses of MS group,especially the changes of responses towards P30-49, P40-60, P89-106,P117-137, P139-161, and P185-206 were significant compared with that the control group only responded to two polypeptides, which indicated that the antigen epitope of MBP, PLP, M87-106, P95-117, P40-60, and P185-206 might have significance in the triggering of MS autoimmune responses.CONCLUSION: TCL induced by MS myelin sheath has different proliferation towards antigen components of myelin sheath from control group. Delipidated myelin sheath significantly increases TCL proliferation in MS group, which suggests that if MS patients developed abnormal degrease in myelin sheath, TCL would produce autoimmune response towards self-myelin sheath, MBP, PLP and its polypeptide segments all can trigger MS or aggravate the state of the illness. Our finding supports the hypothesis of MS autoimmune pathogenic mechanism.
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Objective To investigate the correlation between the plasma homocysteine(Hcy) level and the plaque and its degree of the carotid atherosclerosis (CAS) in elderly patients with acute cerebral infarction (ACI).Methods 93 definit ACI patients recieved the colour Doppler ultrasonograph to detect the intima-media thickness (IMT) of bilateral carotid arteries. Then, the patients were divided into group with CAS plaque(60 cases) and group without CAS plaque(33 cases) according to the result of the detection. Also the degree of CAS were divided to 0～4 levels. The concentration of plasma Hcy of all the patients were measured by enzymatic cycling assay. The correlation analysis was made between plasma Hcy levels and the CAS plaque and the degree of CAS.Results The concentration of plasma Hcy in the group with CAS plaque[18.83 (15.20～24.03)?mol/L] was significantly higher than that in group without CAS plaque[12.30 (9.70～15.10) ?mol/L](P