Shieh Ying-Hua |
------>authors3_c= ------>paper_class1=2 ------>Impact_Factor=None ------>paper_class3=0 ------>paper_class2=0 ------>vol= ------>confirm_bywho=shiemin ------>insert_bywho=syh001 ------>Jurnal_Rank=None ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=24 ------>paper_class2Letter=None ------>page2= ------>medlineContent= ------>unit=E0122 ------>insert_date=20061221 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c=??? ------>score=-40 ------>journal_name=2006???????????????? ------>paper_name=Apotosi?Immuno-modulatory effect ------>confirm_date=20071127 ------>tch_id=079010 ------>pmid=19917714 ------>page1= ------>fullAbstract=Fasciola hepatica is a helminth pathogen that drives Th2/Treg immune responses in its mammalian host. The parasite releases a large number of molecules that are critical to inducing this type of immune response. Here we have selected recombinant forms of two major F. hepatica secreted molecules, the protease cathepsin L (rFhCL1) and anti-oxidant, sigma class glutathione transferase (rFhGST-si), to examine their interactions with dendritic cells (DCs). Despite enzymatic and functional differences between these molecules, both induced IL-6, IL-12p40 and MIP-2 secretion from DCs and enhanced CD40 expression. While this induction was mediated by toll-like receptor 4 (TLR4), their subsequent intracellular signalling pathways differed; rFhCL1 signalled through p38 and rFhGST-si mediated its effect via JNK, p38, p-NF-kappaBp65 and IRF5. Neither rFhCL1 nor rFhGST-si enhanced DC phagocytosis or induced Th2 immune responses in vivo. However, DCs matured in the presence of either enzyme attenuated IL-17 production from OVA-specific T-cells in vivo. In addition, DCs exposed to either antigen secreted reduced levels of IL-23. Therefore, both F. hepatica FhCL1 and FhGST-si modulate host immunity by suppressing responses associated with chronic inflammation - an immune modulatory mechanism that may benefit the parasites survival within the host. ------>tmu_sno=None ------>sno=14454 ------>authors2= ------>authors3= ------>authors4= ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Shieh Ying-Hua ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=1 ------>updateTitle=Major secretory antigens of the helminth Fasciola hepatica activate a suppressive dendritic cell phenotype that attenuates Th17 cells but fails to activate Th2 immune responses. ------>language=1 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2006 ------>submit_flag=None ------>publish_month=9 |