02 BOOK OF ABSTRACTS .indd

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Microscopic techniques approach in studying protease inhibitor cystatin in immune cells Tina Zava{nik-Bergant 1 , Martina Bergant 2 , Ur{ka Repnik 1 , Gareth Griffiths 3 , Rok Romih 4 , Matja` Jeras 2 , Janko Kos 5 , and Vito Turk 1 1 Department of Biochemistry and Molecular Biology, Jo`ef Stefan Institute, Ljubljana, Slovenia; 2 Tissue Typing Center, Blood Transfusion Center of Slovenia, Ljubljana, Slovenia; 3 European Molecular Biology Laboratory (EMBL), Heidelberg, Germany; 4 Institute of Cell Biology, Medical Faculty, University of Ljubljana, Slovenia; 5 Faculty of Pharmacy, University of Ljubljana, Slovenia Dendritic cells possess a big capacity to elicit immune response. Their maturation occurs as they migrate from peripheral tissues to lymphoid organs, where they present captured antigens to T cells. The central role of endosomal/lysosomal proteolytic enzymes in generating antigenic peptides and controlling MHC II traffic defines these enzymes as an important area of investigation. The involvement of natural protease inhibitors has been supported by the study on the cystatin homologue, secreted from filiar parasite, which was shown to down-modulate MHC II-restricted antigen presentation. Our study has been predominantly focused on human cystatin C expressed in dendritic cells in response to their differentiation and activation Dendritic cells are represented as a cell model in which a combination of confocal microscopy and quantitative electron microscopy was successfully applied in order to study endogenous and added cystatin C. We have shown that in immature dendritic cells cystatin C content was highly elevated compared to their precursors. The low content of cystatin C in monocytes resulted from lower expression, but not from its elevated secretion. Increased expression of cystatin C 36l21 and high content in Golgi apparatus were observed in immature dendritic cells. The transport of cystatin C was shown from Golgi apparatus towards the cell membrane, where cystatin C accumulated in fully mature dendritic cells. Differentiation and maturation dependence of endogenous cystatin C supports its intracellular regulatory potential and further suggests it new role in Golgi apparatus of immature dendritic cells.
CpG oligonucleotides admixed with irradiated tumor cells are highly efficient for the tumor prevention but less effective for the treatment of existing tumors Vida Stegel 1 , Andreja Kopitar 2 , Alojz Ihan 2 , Srdjan Novakovi} 1 1 Institute of Oncology Ljubljana, Department of Molecular Diagnostics, Zalo{ka 2, 1000 Ljubljana, Slovenia; 2 Medical Faculty, Institute of Microbiology and Immunology, Korytnikova 2, 1000 Ljubljana, Slovenia The CpG oligonukleotides could be used as immunostimulators that help the maturation of dendritic cells - DC and lymphocytes, and consequently help to trigger an antitumor immune response. The aim of our study was to assess the effectiveness of tumor vaccines composed of irradiated B-16 tumor cells and CpG when used for the prevention of tumor development or for treatment of i.p. B16 tumors. The prevention efficacy was assessed in the experiments that were performed on the intraperitonel (i.p.) B-16 mouse tumor model. The vaccines were administered once or three times i.p. The average survival (AM±SD) of control animals (mock treated) was 21.6±2.5 days. The average survival in the group of animals pretreated with irradiated tumor cells alone was 26.6±3.7 days. The 100-days-overall survival of animals pretreated once with irradiated B16 and 10 µg, 30 µg or 90 µg per animal of CpG was 57%, 30% and 28% respectively. In the very same groups, the average survival of the mice that ultimately died because of tumors was 43.3±33.0, 30.0±15.2 and 42.0±10.7 days, respectively. When the animals were pretreated with the irradiated tumor cells and 10µg, 30µg or 90µg of CpG per animal followed by two repeated injections of CpG only, the 100-days-overall survival was 88%, 100% and 100% respectively. l22 37 In the second set of experiments, the effect of the vaccine on already established tumors was followed. The animals were first i.p. challenged with viable tumor cells, and on the second day, treated with CpG and irradiated tumor cells. The average survival in the group of animals treated with irradiated tumor cells alone was 20.0±9.8 days. The average survival of animals treated with one injection of 30µg of CpG per animal was 21.0±7.2 days, while the average survival of animals treated with three repeated injections of 30µg of CpG was 24.0±6.7 days. Similarly to achievements in the previous groups, the treatment with one dose of irradiated tumor cells and one injection of 30µg of CpG per animal resulted with no long-term survivors. Average survival in this group was 21.0±6.4 days. Among the animals treated with the irradiated tumor cells and 30µg of CpG per animal followed by two repeated injections of CpG only, 18% of animals survived more then 100 days. The average survival of the mice that ultimately died because of tumors was 28.0±12.2 days. In conclusion, the tumor vaccine composed of irradiated B16 tumor cells and CpG delays the B16 tumor development and, to a great extent, protects the animals against tumor development. The curative treatment capacity of this kind of vaccine is limited with the size of the tumor mass. Therefore, the tumor vaccine is more useful for the prevention of tumor development than for the treatment of existing tumors.
Page 2 and 3: Co-chairs of the conference: Scient
Page 4 and 5: Contents Conference programme 5 Lis
Page 6 and 7: Differential effects of Cathepsin L
Page 8 and 9: 17.25 - 17.50 Golzio Muriel, IPBS C
Page 10 and 11: List of lectures: L1. Teissiè Just
Page 13 and 14: Abstracts of lectures 13
Page 15 and 16: Proteases and their inhibitors duri
Page 17 and 18: Biochemical characterization and cl
Page 19 and 20: Assessment of cathepsin B activity
Page 21 and 22: Differential effects of Cathepsin L
Page 23 and 24: anecdotally and within a clinical t
Page 25 and 26: Tumor cell- and macrophage-derived
Page 27 and 28: The selection of serological marker
Page 29 and 30: Cathepsins and their inhibitors in
Page 31 and 32: Matrix metalloproteinase expression
Page 33 and 34: l18 33 Complement resistance impair
Page 35: Classical tumor vaccine potently st
Page 39 and 40: Electrochemotherapy in veterinary o
Page 41 and 42: studies were able to provide a deta
Page 43 and 44: threshold and electric field intens
Page 45 and 46: Gene delivery systems in cancer gen
Page 47 and 48: Electropermeabilization: a non vira
Page 49 and 50: Visible light microscopy, efficient
Page 51 and 52: Progress in tumour vascular targeti
Page 53 and 54: The Fer kinas: a novel target for p
Page 55 and 56: Targeting of plasminogen activation
Page 57 and 58: Functional interdependence of natur
Page 59 and 60: Antiprotease therapy in cancer: hot
Page 61 and 62: Functional genomics and systems bio
Page 63 and 64: Tumor proteolysis: a multidimension
Page 65 and 66: Stem cell therapy for liver insuffi
Page 67 and 68: Increased plasma DNA concentration
Page 69 and 70: List of poster presentations P1. Ab
Page 71 and 72: Abstracts of posters 71
Page 73 and 74: Tumor VEGF modulates host proteolyt
Page 75 and 76: New inhibitors of human hydroxyster
Page 77 and 78: Cytotoxicity and antitumour effecti
Page 79 and 80: Quantification of lysosomal fusion
Page 81 and 82: Spatiotemporal relevance of tumor c
Page 83 and 84: Electrogene therapy with p53 alone
Page 85 and 86: Do organophosphorous pesticides pla
Page 87 and 88:
Molecular analysis of lymphoprolife
Page 89 and 90:
Humoral response in pleural space t
Page 91 and 92:
In conclusion, this study shows tha
Page 93 and 94:
Angiogenesis correlates with cycloo
Page 95 and 96:
Inhibition of mouse uPA activity by
Page 97 and 98:
Cathepsin X interacts with integrin
Page 99 and 100:
Annexin-V apoptosis analysis of hum
Page 101 and 102:
Tissue swelling at the site of elec
Page 103 and 104:
p30103 The Bcl-2 family members: me
Page 105 and 106:
p32105 Proteomics of astrocytic neo
Page 107 and 108:
Correlation of chromosomal abnormal
Page 109 and 110:
Optimization of treatment parameter
Page 111 and 112:
The effect of xantohumol on normal
Page 113 and 114:
Cappabianca Lucia University of Aqu
Page 115 and 116:
Jevnikar Zala University of Ljublja
Page 117 and 118:
Mesojednik Suzana Institute of Onco
Page 119 and 120:
Rols Marie-Pierre Institute of Phar
Page 121 and 122:
Author Index Abramovi} Zrinka 72 Ak
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Paridaens R. 31 Parker Katharine 99
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02 BOOK OF ABSTRACTS .indd

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