Viral Immune Modulation
A microbial pathogen enters our body - but not unnoticed! Immune cells have specialised receptors to detect the presence of the invaders. These receptors initiate defence mechanisms as soon as the pathogen has entered the body – unless they are disarmed.
Our immune system has two main defence lines to eliminate pathogens entering our body: the innate and the adaptive immune system. While the latter leads to a precisely coordinated defence of the pathogen days after infection, the innate immune response acts at the very beginning of the infection right after invasion of our body.
Toll-like receptors (TLRs) are part of the innate immune response against microbial pathogens. They reside in various immune cells and recognize conserved structures of pathogenic organisms such as certain surface molecules, DNA motifs or proteins.
Herpes viruses establish lifelong infections and are masters of immune evasion. They interfere with the adaptive immune response at many levels, but little is known about herpes viral modulation of the innate immune response. Toll-like receptor 9 plays a pivotal role for the detection of herpes viruses and induces a potent antiviral interferon response. The cellular UNC93B protein is essential for proper functioning of TLR9: it delivers TLR9 from the endoplasmic reticulum, where it is synthesized and stored until needed, to a specialized intracellular compartment called the endosome. There, TLR9 meets the DNA of the invading pathogen and initiates a signalling cascade that results in the activation of an antiviral response. Whereas the downstream signalling cascade of TLRs is well characterised, little is known about the regulation of intracellular trafficking in infected antigen presenting cells.
One focus of the research group “Viral Immune Modulation” is to study the regulation of intracellular trafficking of TLR9 upon infection with herpes viruses. Using fluorescently labelled virions and fluorescently labelled TLR9 and UNC93B proteins, the group will analyse intracellular trafficking in real-time in primary antigen presenting cells. The researchers have evidence that herpes viruses can evade the antiviral response initiated by TLRs. They aim to identify the responsible herpes viral genes and characterise their mechanism of action in order to deepen our understanding of herpes viral infections and the host’s immune response.
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