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This master's thesis studies the efficacy of cancer immunotherapy based on TLR agonists and ligands stimulating phagocytosis, abbreviated as MBTA therapy, using a mouse model of pancreatic adenocarcinoma. The main goals are: (1) to enhance the efficacy of MBTA in the case of large tumors, (2) to enhance the efficacy of MBTA using a bilateral pancreatic adenocarcinoma mouse model, (3) to examine the potential of lipoteichoic acid to opsonize cancer cells and stimulate phagocytic cells.

The aim of this thesis is to improve the therapeutic effect of the immunotherapy based on the synergy of TLR agonists with phagocytosis stimulating ligands. Furthermore, this thesis is focused on the information transfer to the specific immunity, as well as it pursues the study of the specific immunity relevance during cancer immunotherapy.

The aim of this thesis was to study cancer immunotherapy based on combination of TLR7 signalling and activation of phagocytosis of cancer cells. This thesis was focused on the possibility of enhancing its effect. The possibilities of removing immunosuppressive barriers (esp. MDSCs and adenosine) were studied, using a combination with chemotherapy or enzyme - adenosine deaminase and purine nucleoside phosphorylase. The effect of enzymes was studied in both in vivo and in vitro experiments. As another way of optimizing the therapy used so far, the modulation of the therapeutic mixture using lower molecular weight substances was tried.

The aim of this thesis was to study how to increase effectiveness of cancer immunotherapy based on synergy of compounds stimulating phagocytosis and TLR agonist. Tumor microenvironment was modified by enzymes, which catalised conversion of lactate to pyruvate or acetate. It was monitored effect of enzymes on tumor size, survival of experimental mice and cytotoxicity on tumor cells.

The main aim of this thesis was to study the role of regulatory T cells in cancer. Their presence, importance, and mechanism of their action were studied as well. The practical part was focused on reduction of bigger tumors and suppressing regulatory T-cell effects. The combination of TLR agonists, agonistic CD40 antibody and anti-CTLA-4 was studied on a mouse model of pancreatic adenocarcinoma.

The aim of this thesis was to study murine melanoma B16-F10 therapy based on activation of both innate immune system and acquired immunity. The practical part was designed as an optimization of the therapy based on combination of TLR signalling and activation of phagocytosis of cancer cells. Mechanisms of therapeutic cancer vaccines and the influence of the therapy on parallel untreated tumor were studied as well.

The aim of this thesis was to study cancer immunotherapy based on combination of TLR7 signalling and activation of phagocytosis of cancer cells. We studied the influence of our immunotheraphy on parallel untreated tumor. Mechanisms of therapy were studied in vitro. The possibility to enhance therapeutic effect using more complex mixture of TLR agonists was studied as well.