Thesis supervisor: Gergely Nagy
Location of studies (in Hungarian): University of Debrecen Abbreviation of location of studies: DEÁOK
Description of the research topic:
Macrophages are key components of the immune system. Their primary role is tissue sampling, namely the uptake and processing of tissue debris and pathogens and then presenting the antigens to helper T cells. Macrophages can adapt to any tissue environment, and in the case of tissue damage or infection, they take part in both pro-inflammatory processes and the resolution of inflammation. The former cell type is called M1-type or classically polarized macrophage.
The macrophage phenotype is formed by well-known lineage-determining factors like PU.1 (ETS superfamily) with IRF4/8 (IRF family), C/EBP, AP-1 (bZIP superfamily), and RUNX1 proteins (RUNX family). Besides, additional bZIP and bHLH proteins, nuclear receptors, and MEF2 proteins contribute to gene regulation in different tissue macrophages.
During classical polarization, additional players of the macrophage transcription factor network turn on, out of which the first and most important one is NFkB. Our goal is to understand how NFkB disturb and direct the gene regulatory processes leading to M1-type macrophages using bioinformatics tools.
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