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MBD2 Promotes Th17 Differentiation in Severe Asthma Via Modulating SOCS3 Expression
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A2485 - MBD2 Promotes Th17 Differentiation in Severe Asthma Via Modulating SOCS3 Expression
Author Block: W. Sun1, X. Xiang2; 1Department of Respiratory Medicine,the Second Xiangya Hospital, Central South University, Changsha, China, 2Department of Emergency,the Second Xiangya Hospital, Central South University, Changsha, China.
RATIONALE: To investigate the expression of methtyl-CpG binding domain protein 2(MBD2) and suppressor of cytokine signaling 3(SOCS3) in severe asthmatic mice and explore whether MBD2 promoted the Th17 cell differentiation through SOCS3.
METHODS: We established a murine model that mimic the Th17 cell-dependent, neutrophil-dominant airway inflammation of severe asthma. The pathological changes of lung tissues were observed by HE staining, immunohistochemistry of neutrophils and eosinophils. Th17 cell differentiation were detected by flow cytometry, expression of MBD2, SOCS3, STAT3, pSTAT3 and RORγt were detected by quantitative Real-Time PCR(qRT-PCR) and western blotting. In vitro, We used siRNA to overexpression or silencing MBD2 or SOCS3 gene in Splenic CD4+ T cells, after 72h differentiation of naïve T cells into Th17 cells, cells were collected for detection as described above.
RESULTS: We found that in severe asthmatic mice, in correlation to the Th17 cell and neutrophil infiltration, the MBD2 expression significantly elevated. Also, SOCS3 expression decreased in the severe asthma group, with a concomitant unaffected expression but significantly elevated phosphorylation of STAT3. We further analyzed the impact of SOCS3 intervention on the differentiation of Th0 cells. Knock-down of SOCS3 with siRNA promoted the differentiation of naïve T cells into Th17 cells. As for overexpression or silencing of the MBD2 gene, the differentiation of Th17 cells and IL-17 secretion showed positive changes, SOCS3 protein expression showed a negative change. whereas there was no significant difference in the expression of MBD2 under overexpression or silencing of the SOCS3 gene.
CONCLUSION: These data indicated that MBD2 might facilitate Th17 cell differentiation via modulation of SOCS3, hence promote the pathogenesis of severe asthma.
Author Block: W. Sun1, X. Xiang2; 1Department of Respiratory Medicine,the Second Xiangya Hospital, Central South University, Changsha, China, 2Department of Emergency,the Second Xiangya Hospital, Central South University, Changsha, China.
RATIONALE: To investigate the expression of methtyl-CpG binding domain protein 2(MBD2) and suppressor of cytokine signaling 3(SOCS3) in severe asthmatic mice and explore whether MBD2 promoted the Th17 cell differentiation through SOCS3.
METHODS: We established a murine model that mimic the Th17 cell-dependent, neutrophil-dominant airway inflammation of severe asthma. The pathological changes of lung tissues were observed by HE staining, immunohistochemistry of neutrophils and eosinophils. Th17 cell differentiation were detected by flow cytometry, expression of MBD2, SOCS3, STAT3, pSTAT3 and RORγt were detected by quantitative Real-Time PCR(qRT-PCR) and western blotting. In vitro, We used siRNA to overexpression or silencing MBD2 or SOCS3 gene in Splenic CD4+ T cells, after 72h differentiation of naïve T cells into Th17 cells, cells were collected for detection as described above.
RESULTS: We found that in severe asthmatic mice, in correlation to the Th17 cell and neutrophil infiltration, the MBD2 expression significantly elevated. Also, SOCS3 expression decreased in the severe asthma group, with a concomitant unaffected expression but significantly elevated phosphorylation of STAT3. We further analyzed the impact of SOCS3 intervention on the differentiation of Th0 cells. Knock-down of SOCS3 with siRNA promoted the differentiation of naïve T cells into Th17 cells. As for overexpression or silencing of the MBD2 gene, the differentiation of Th17 cells and IL-17 secretion showed positive changes, SOCS3 protein expression showed a negative change. whereas there was no significant difference in the expression of MBD2 under overexpression or silencing of the SOCS3 gene.
CONCLUSION: These data indicated that MBD2 might facilitate Th17 cell differentiation via modulation of SOCS3, hence promote the pathogenesis of severe asthma.
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