Objective:To investigate the effects of Compound Fufangteng Mixture(CFM)on the expression levels of CD11b^(+)monocytes surface activation molecules CD2,CD69 and depleted molecules PD-1 and CD95 in spleen and periphera...Objective:To investigate the effects of Compound Fufangteng Mixture(CFM)on the expression levels of CD11b^(+)monocytes surface activation molecules CD2,CD69 and depleted molecules PD-1 and CD95 in spleen and peripheral blood of immunosuppressed mice.Methods:30 healthy SPF Balb/c male mice were randomly divided into Control,immunosuppressive model group(CTX group),high,medium and low dose intervention group(CTX+CFM-H group,CTX+CFM-M group,CTX+CFM-L group),Astragalus particles(AP)intervention group(CTX+AP group).The mice in each intervention group were injected intraperitoneally with cyclophosphamide(CTX)70 mg/kg for 3 consecutive days,and then administered for 10 d according to the group regimen,and the materials were taken 24 h after the last dose.Flow cytometry detected the expression of CD11b^(+)monocytes surface activation molecules(CD2,CD69)and depleting molecules(PD-1,CD95)in mouse peripheral blood.Results:Compared with the control group,the expression levels of CD11b^(+)and CD69+in the spleen of CTX+CFM-H,CTX+CFM-M and CTX+CFM-L groups showed an improvement trend,and decreased with the dose gradient of CFM.Conclusion:CFM could regulate the immune function of splenic CD11b+ CD69 cells in immunosuppressed mice.展开更多
The 8^th International Workshop on Human Leucocyte Differentiation Antigens （chaired by HZ and managed by BS） was run over a 4-year period and culminated in a conference in December 2004. Here we review the achievem...The 8^th International Workshop on Human Leucocyte Differentiation Antigens （chaired by HZ and managed by BS） was run over a 4-year period and culminated in a conference in December 2004. Here we review the achievements of the HLDA Workshops and provide links to information on CD molecules and antibodies against them, including the 93 new CDs assigned in the 8^th Workshop. We consider what remains to be achieved （including an estimate of the number of leucocyte surface molecules still to be discovered）, and how the field can best move forward.展开更多
AIM: To investigate and elucidate the molecular mechanism that regulates inducible expression of CD69 by Helicobacter pylori (H. pylori ) infection. METHODS: The expression levels of CD69 in a T-cell line, Jurkat, pri...AIM: To investigate and elucidate the molecular mechanism that regulates inducible expression of CD69 by Helicobacter pylori (H. pylori ) infection. METHODS: The expression levels of CD69 in a T-cell line, Jurkat, primary human peripheral blood mononuclear cells (PBMCs), and CD4 + T cells, were assessed by immunohistochemistry, reverse transcription polymerase chain reaction, and flow cytometry. Activation of CD69 promoter was detected by reporter gene. Nuclear factor (NF)-κB activation in Jurkat cells infected with H. pylori was evaluated by electrophoretic mobility shift assay. The role of NF-κB signaling in H. pylori-induced CD69 expression was analyzed using inhibitors of NF-κB and dominant-negative mutants. The isogenic mutants with disrupted cag pathogenicity island (cag PAI) and virD4 were used to elucidate the role of cag PAI-encoding type Ⅳ secretion system and CagA in CD69 expression.RESULTS: CD69 staining was detected in mucosal lymphocytes and macrophages in specimens of pa- tients with H. pylori-positive gastritis. Although cag PAI- positive H. pylori and an isogenic mutant of virD4 induced CD69 expression, an isogenic mutant of cag-PAI failed to induce this in Jurkat cells. H. pylori also induced CD69 expression in PBMCs and CD4 + T cells. The activation of the CD69 promoter by H. pylori was mediated through NF-κB. Transfection of dominant-negative mutants of IκBs, IκB kinases, and NF-κB-inducing kinase inhibited H. pylori-induced CD69 activation. Inhibitors of NF-κB suppressed H. pylori-induced CD69 mRNA expression. CONCLUSION: The results suggest that H. pylori induces CD69 expression through the activation of NF-κB. cagPAI might be relevant in the induction of CD69 expression in T cells. CD69 in T cells may play a role in H. pylori-induced gastritis.展开更多
基金National Natural Science Foundation Project(No.81860780)Guangxi Natural Science Foundation General Project(No.2020GXNSFAA297162)。
文摘Objective:To investigate the effects of Compound Fufangteng Mixture(CFM)on the expression levels of CD11b^(+)monocytes surface activation molecules CD2,CD69 and depleted molecules PD-1 and CD95 in spleen and peripheral blood of immunosuppressed mice.Methods:30 healthy SPF Balb/c male mice were randomly divided into Control,immunosuppressive model group(CTX group),high,medium and low dose intervention group(CTX+CFM-H group,CTX+CFM-M group,CTX+CFM-L group),Astragalus particles(AP)intervention group(CTX+AP group).The mice in each intervention group were injected intraperitoneally with cyclophosphamide(CTX)70 mg/kg for 3 consecutive days,and then administered for 10 d according to the group regimen,and the materials were taken 24 h after the last dose.Flow cytometry detected the expression of CD11b^(+)monocytes surface activation molecules(CD2,CD69)and depleting molecules(PD-1,CD95)in mouse peripheral blood.Results:Compared with the control group,the expression levels of CD11b^(+)and CD69+in the spleen of CTX+CFM-H,CTX+CFM-M and CTX+CFM-L groups showed an improvement trend,and decreased with the dose gradient of CFM.Conclusion:CFM could regulate the immune function of splenic CD11b+ CD69 cells in immunosuppressed mice.
文摘The 8^th International Workshop on Human Leucocyte Differentiation Antigens （chaired by HZ and managed by BS） was run over a 4-year period and culminated in a conference in December 2004. Here we review the achievements of the HLDA Workshops and provide links to information on CD molecules and antibodies against them, including the 93 new CDs assigned in the 8^th Workshop. We consider what remains to be achieved （including an estimate of the number of leucocyte surface molecules still to be discovered）, and how the field can best move forward.
文摘AIM: To investigate and elucidate the molecular mechanism that regulates inducible expression of CD69 by Helicobacter pylori (H. pylori ) infection. METHODS: The expression levels of CD69 in a T-cell line, Jurkat, primary human peripheral blood mononuclear cells (PBMCs), and CD4 + T cells, were assessed by immunohistochemistry, reverse transcription polymerase chain reaction, and flow cytometry. Activation of CD69 promoter was detected by reporter gene. Nuclear factor (NF)-κB activation in Jurkat cells infected with H. pylori was evaluated by electrophoretic mobility shift assay. The role of NF-κB signaling in H. pylori-induced CD69 expression was analyzed using inhibitors of NF-κB and dominant-negative mutants. The isogenic mutants with disrupted cag pathogenicity island (cag PAI) and virD4 were used to elucidate the role of cag PAI-encoding type Ⅳ secretion system and CagA in CD69 expression.RESULTS: CD69 staining was detected in mucosal lymphocytes and macrophages in specimens of pa- tients with H. pylori-positive gastritis. Although cag PAI- positive H. pylori and an isogenic mutant of virD4 induced CD69 expression, an isogenic mutant of cag-PAI failed to induce this in Jurkat cells. H. pylori also induced CD69 expression in PBMCs and CD4 + T cells. The activation of the CD69 promoter by H. pylori was mediated through NF-κB. Transfection of dominant-negative mutants of IκBs, IκB kinases, and NF-κB-inducing kinase inhibited H. pylori-induced CD69 activation. Inhibitors of NF-κB suppressed H. pylori-induced CD69 mRNA expression. CONCLUSION: The results suggest that H. pylori induces CD69 expression through the activation of NF-κB. cagPAI might be relevant in the induction of CD69 expression in T cells. CD69 in T cells may play a role in H. pylori-induced gastritis.
