经鼻黏膜给予MBP6886和8799协同免疫预防Lewis大鼠EAE的实验研究
鼻黏膜耐受;,MBP6886;,MBP8799;,实验性自身免疫性脑脊髓炎,,]鼻黏膜耐受;,MBP6886;,MBP8799;,实验性自身免疫性脑脊髓炎,1材料和方法,2结果,3讨论,参考文献:
Inhibiton of experimental autoimmune encephalomyelitis in Lewis rats by nasal administration of encephalitogenic MBP peptides:synergisticeffectsofMBP6886 and 8799SUN Bo, YANG Shuo, PENG Haisheng, QIAO Hui, CAO Jingyan, JIN Lianhong, LI Hulun*
DepartmentofNeurobiology,ProvinceNeurobiologyKeyLaboratory,HarbinMedical University,Harbin 150086, China
[Abstract] AIM: To explore the synergistic effect of MBP6886 and 8799, on the inhibition of experimental autoimmune encephalomyelitis (EAE) in Lewis rat by nasal administration. METHODS: Three different MBP peptides(MBP6886, 8799, and the nonencephalitogenic peptide 110128) were synthesized and administrated nasally to Lewis rat on day11, 10, 9, 8 and 7 prior to immunization with the guinea pig MBP (gpMBP) + CFA, which was used to induce EAE. The protective effect on Lewis rat from EAE by the MBP peptides was evaluated. RESULTS: Protection was achieved with the encephalitogenic peptides MBP6886 and 8799, MBP6886 being more potent, but not with MBP110128. Neither MBP6886 nor 8799 used alone conferred complete protection to gpMBPinduced EAE. In contrast, nasal administration of a mixture of MBP6886 and 8799 completely blocked gpMBPinduced EAE even at lower dosage than being used alone. Rats tolerized with MBP6886+8799 nasally showed decreased T cell responses to MBP, reflected by lymphocyte proliferation and IFNγ ELISPOT assays. Rats tolerized with MBP6886+8799 also had abrogated MBPreactive IFNγ and TNFα mRNA expression in lymph node cells compared to rats receiving MBP110128 nasally, while similar low levels of MBPreactive TGFβ and IL4 mRNA expressing cells were observed in the two groups. CONCLUSION: Nasal administration of encephalitogenic MBP peptides can induce antigenspecific T cell tolerance and confer incomplete protection to gpMBPinduced EAE, and MBP 6886 and 8799 have synergistic effecs. Nonregulatory mechanisms are proposed to be responsible for tolerance development after nasal peptide administration. ......
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