AIM: To observe the change of periphery and centra CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg of MOG₃₅₋₅₅; induced EAE disease in mouse, and to explore the potential mechanism of cellular immunity in the process of EAE. METHODS: MOG₃₅₋₅₅; were used to establish EAE model on femina C57BL/6 mice.The behavioral changes and the histological scores were recorded. The changes of CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg on periphery and centra lymphocyte in spleen , brain were analyzed by flow cytometry. RESULTS: MOG₃₅₋₅₅;-induced EAE group Showed the typical clinical behavior and pathological manifestations, CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg lymphocytes were detected in the brain and spinal cord of EAE group mice, but they were not detected in the brain of control group. CD8(+); CD28(-); Treg in the spleen of EAE group were lower than those in control group (P < 0.01). CD4(+); CD25(+); Treg lymphocytes were slight higher than the control group. CONCLUSION: CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg lymphocytes all play important roles in the pathogenesy of EAE. The distribution of CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg in the CNS and peripheral of EAE is different, suggesting that their entry into the CNS and regulate of local inflammation.
AIM: To observe the change of periphery and centra CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg of MOG₃₅₋₅₅; induced EAE disease in mouse, and to explore the potential mechanism of cellular immunity in the process of EAE. METHODS:MOG₃₅₋₅₅; were used to establish EAE model on femina C57BL/6 mice.The behavioral changes and the histological scores were recorded. The changes of CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg on periphery and centra lymphocyte in spleen , brain were analyzed by flow cytometry. RESULTS:MOG₃₅₋₅₅;-induced EAE group Showed the typical clinical behavior and pathological manifestations, CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg lymphocytes were detected in the brain and spinal cord of EAE group mice, but they were not detected in the brain of control group. CD8(+); CD28(-); Treg in the spleen of EAE group were lower than those in control group (P < 0.01). CD4(+); CD25(+); Treg lymphocytes were slight higher than the control group. CONCLUSION:CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg lymphocytes all play important roles in the pathogenesy of EAE. The distribution of CD4(+); CD25(+); Treg, CD8(+); CD28(-); Treg in the CNS and peripheral of EAE is different, suggesting that their entry into the CNS and regulate of local inflammation.