Publications by authors named "H PRIBYLOVA"

CD4(+)CD25(+)Foxp3(+) T regulatory cells (Tregs) and CD1d-restricted invariant natural killer T (iNKT) cells are two cell types that are known to regulate immune reactions. Depletion or inactivation of Tregs using specific anti-CD25 antibodies in combination with immunostimulation is an attractive modality especially in anti-tumour immunotherapy. However, CD25 is not expressed exclusively on Tregs but also on subpopulations of activated lymphocytes.

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Downregulation of MHC class I expression on the cell surface is a common mechanism by which tumour cells, including cervical carcinoma, can escape the T cell-mediated anti-tumour immunity. This downregulation represents an obstacle for the efficacy of anti-tumour vaccines. In this study, we investigated the efficacy of prophylactic peptide and peptide-pulsed dendritic cell-based vaccines in a murine model of experimental MHC class I-deficient tumours (TC-1/A9), expressing E6/E7 oncogenes derived from HPV16, and compared the efficacy of particular vaccination settings to anti-tumour protection against parental MHC class I-positive TC-1 tumours.

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Background: Intensive selfmonitoring is an important and cost-demanding part of diabetes treatment. Continuous glucose monitoring (CGM) using transcutaneous sensors offers "real time" information on glycemia. In the present study, we assessed the therapeutic efficacy of CGM on metabolic control using two different statistical methods: linear regression and "survival analysis".

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Aims: There is no standardized protocol for measuring glycemic index (GI) that takes time-of-day effects into account. The software DegifXL2 and Medtronic-Minimed's CGMS and Solutions, makes the GI calculation at breakfast and dinner time possible. The aim of this study was to assess the enhanced data processing software (DegifXL4) enabling the GI calculation at breakfast, lunch, afternoon snack and dinner times.

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Epigenetic events play an important role in tumour progression and also contribute to escape of the tumour from immune surveillance. In this study, we investigated the up-regulation of major histocompatibility complex (MHC) class I surface expression on tumour cells by epigenetic mechanisms using a murine tumour cell line expressing human E6 and E7 human papilloma virus 16 (HPV16) oncogenes and deficient in MHC class I expression, as a result of impaired antigen-presenting machinery (APM). Treatment of the cells with the histone deacetylase inhibitor Trichostatin A, either alone or in combination with the DNA demethylating agent 5-azacytidine, induced surface re-expression of MHC class I molecules.

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