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  • 1.
    Gasperov, Nina Milutin
    et al.
    Division of Molecular Medicine, Rudjer Boskovic Institute, Zagreb, Croatia.
    Farkas, Sanja A.
    Örebro University Hospital. Department of Laboratory Medicine, Örebro University Hospital, Örebro, Sweden.
    Nilsson, Torbjörn K.
    Department of Medical Biosciences, Unit of Clinical Chemistry, Umeå University, Umeå, Sweden.
    Grce, Magdalena
    Division of Molecular Medicine, Rudjer Boskovic Institute, Zagreb, Croatia.
    Epigenetic activation of immune genes in cervical cancer2014In: Immunology Letters, ISSN 0165-2478, E-ISSN 1879-0542, Vol. 162, no 2, p. 256-257Article in journal (Refereed)
    Abstract [en]

    Immune system provides us protection from infectious pathogens and tumors formation during lifetime. Cervical cancer (CC), and its cause, human papillomavirus (HPV) are both challenges for the immune system. We present here evidence of epigenetic activation of immune system genes in CC. Illumina Infinium Human Methylation 450 K BeadChip identified genes, which were all significantly hypomethylated in CC tissue versus normal tissue. The GeneMANIA computer program identified a tight network between those genes. The most strongly correlated genes based on their function are immune effectors' process (AIM2, BST2, BTN3A3, and IL12RB1) and response to virus related genes (AIM2, BST2, and IL12RB1). Thus, activation of those genes through demethylation is probably triggered by HPV oncogenes. In conclusion, the immune system of women who do not develop CC is probably activated earlier through DNA demethylation.

  • 2.
    Skoglund, Caroline
    et al.
    Department of Biomedicine, School of Health and Medical Sciences, Örebro University, Örebro, Sweden; Division of Molecular Surface Physics and Nanoscience, Department of Physics, Chemistry and Biology, Linköping University, Linköping, Sweden.
    Wettero, Jonas
    Rheumatology/Autoimmunity and Immune Regulation Unit (AIR), Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Bengtsson, Torbjörn
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Biomedicine, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    C1q regulates collagen-dependent production of reactive oxygen species, aggregation and levels of soluble P-selectin in whole blood2012In: Immunology Letters, ISSN 0165-2478, E-ISSN 1879-0542, Vol. 142, no 1-2, p. 28-33Article in journal (Refereed)
    Abstract [en]

    Blood platelets express several receptors involved in immunity (e.g. complement-, toll-like- and Fc gamma-receptors) and release inflammatory mediators. Furthermore, formation of platelet-leukocyte aggregates has an important role during inflammatory conditions such as coronary artery disease. Thus, apart from their well-known role in haemostasis, platelets are today also recognized as cells with immunomodulatory properties. We have previously reported regulatory effects of complement protein 1q (C1q) on platelet activation in experimental setups using isolated cells. In the present study we have proceeded by investigating effects of C1q on collagen-induced aggregation, production of reactive oxygen species (ROS), formation of platelet-leukocyte aggregates and levels of soluble P-selectin in whole blood. Impedance measurements showed that C1q inhibited collagen-induced aggregation whereas it potentiated the collagen-provoked production of ROS in a luminol-dependent chemiluminescence assay. The effects of C1q on aggregation and ROS-production were dependent upon platelets, as they were no longer observed in presence of the platelet (GpIIb/IIIa) inhibitor Reopro. Furthermore, the levels of soluble P-selectin were found to be lowered upon treatment with C1q prior to addition of collagen. There was also a trend towards a decreased formation of large platelet-leukocyte aggregates in collagen-stimulated whole blood following C1q treatment. In conclusion, our data indicate that C1q could have a role in regulating platelet activation and associated leukocyte recruitment during vessel wall injury. This has implications for inflammatory disorders such as coronary artery disease.

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