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The Relation Between NF-κB on Regulation of Dendeitis Cell and Imbalance of T Helper Cell Differentiation in the Pathogenesis of Henoch-schonlein Purpura

Author: TaoHong
Tutor: LiQiu
School: Chongqing Medical University
Course: Pediatrics
Keywords: Dendritic cells T lymphocytes Henoch-Schonlein purpura Nuclear factor-kappa B Henoch-Schonlein purpura Nephritis
CLC: R554.6
Type: Master's thesis
Year: 2010
Downloads: 62
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Abstract

PARTⅠTHE RELATION OF DENDRITIC CELL TO THE IMBALANCE DIFFERENTIATION FO T HELPER CELL IN PATHOGENESIS OF HENOCH-SCHONLEIN PURPURAObjective: Discussion the relation between the abnormal regulation signals of dendritic cells(DC) and the dysimmunity of pathogenesis of Henoch-Schonlein purpura (HSP).Methods: Immunoglobulin Levels were detected by nephelom etry assay in children with HSP . Inflammatory cytokines IL-4, INF-γin blood plasma and IL-12, IL-10 in the supernatants of cultured DC were detected by ELISA. The count of CD86, CD80, CD83, HLA-DR, CD-209 expressed on DC were detected by cell flow cytometry.Results: HSP group showed: The levels of plasma IgA and IgE were higher than the control group, IL-12 levels in the supernatants of cultured DC and INF-γlevels in the plasma were lower than the control group,IL-10 levels in the supernatants of cultured DC and IL-4 levels in the plasma were significantly increased than the control group. CD86, CD83, HLA-DR expressed on DC were significantly higher and CD80 was significantly lower than the control group, P<0.05. CD-209 of Two groups had no statistical significance, P>0.05.Conciusion: The anomalies of antigenspecific signals, costimulatory signals and differentiation or polarization signal of DC might be involved in Th1/Th2 imbalance and synthesis of abnormal immunoglobulins in pathogenesis HSP.PARTⅡNF-κB- DC–Th CELL SIGNALING PATHWAY IN THE ROLEOF IN PATHOGENESIS OF HENOCH-SCHONLEIN PURPURAObjective :To investigate The relation between nuclear transcription factor-κB on regulation of dendritic cell and imbalance of T helper cell differentiation in the pathogenesis of Henoch-Schonlein purpura.Methods :Inflammatory cytokines IL-12,IL-10 in the supernatants of cultured DC were detected by ELISA. The cell count of CD86,CD80,CD83,HLA-DR,CD-209 expression on DC were determined by cell flow cytometry. RT-PCR detection of NF-κB isoforms p50,p65mRNA expression.cells immunohistochemical detection the abnormal NF-κB expression in DC. Detection of the control group, HSP and HSPN patients did not join the NF-ΚB inhibitor BAY-11-7082 and added inhibitors, the above indicators of change.Results: Compared with the control group, DC cultured in HSP and HSPN group showed: IL-12 levels in the supernatants of cultured DC lower than the control group,IL-10 levels in the supernatants of cultured DC was significantly increased than the control group;CD86,CD83, HLA-DR was significantly higher but CD80 was significantly lower than the control group.NF-κB p50,p65 mRNA expression intracellular also increased,and had a large number of NF-κB activation. HSP and HSPN group detected had no statistical relationship between the above, When NF-κB inhibitors to join most of the above indicators are back to normal.Conclusion :The function of Th1 was decreased while the function of Th2 was increased in HSP,which were related to DC abnormal discussion.NF-κB is a key regulatory genes of DC immune function , inhibit activation of NF-κB is a valid target to blocking DC function and depends on the T-cell immune response,It will be an effective way to treatment HSP earlier.

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CLC: > Medicine, health > Internal Medicine > Blood and lymphatic system diseases > Blood diseases > Hemorrhagic disease > Purpura
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