Regulation Of CTLA-4and BLTA By MiR-155in A Mouse Model Of Asthma

ObjectiveTo investigate the mechanism of miRNA-155regulating expression of T lymphocytecytokine in the pathogenesis of asthma.MethodsAsthma was induced in mice, and basal expression of miRNA-155and co-stimulatedmolecular--CTLA-4, BTLA, and Th1, Th2lymphocyte cytokine was measured in asthmamice.Asthma mice were transfected via lentiviral transduction with gene sequence encodedby miRNA-155, so as to induce upregulation of expression of miRNA-155. And expressionof CTLA-4, BTLA and Th1, Th2lymphocyte cytokine was observed. Then siRNAsequence was transfected into asthma mice to induce surpression of miRNA-155in asthmamice, and expression of CTLA-4, BTLA and Th1, Th2lymphocytes cytokine wasanalyzed.Result：In asthma mice model, elevated expression of miRNA-155was observed in CD4~+Tcell, which was transfected with lentivirus whose gene sequence was encoded bymiRNA-155. Surpression of CTLA-4and upregulation of Th1, Th2lymphocyte cytokinewas also observed while there was no significnat change in expression of BTLA.Meanwhile, in asthma mice transfected with lentivirus carried miRNA-155siRNA,surpression of miRNA-155in CD4+T cell and Th1,Th2lymphocyte cytokine wasobserved while CTLA-4was found upregulated and no significant change was observed inexpression of BTLA.ConclusionExpression of CTLA-4was negatively regulated by miRNA-155at post-trans-criptional level, thus expression of Th1, Th2lmphocyte cytokine was also regulated. Upregulation of CTLA-4was induced by surpression of miRNA-155, therefore inhibitedsecretion of T lymphocyte cytokine of asthma patients.