Min Ae Lee-Kirsch Group
Molecular genetics of autoinflammatory and autoimmune diseases
Our group focuses on the molecular mechanisms that underlie autoinflammation and autoimmunity and that are caused by perturbations of the type I interferon (IFN) axis. Type I IFNs play a pivotal role in the first line of defense against viral infections. Activation of type I IFN signaling is induced by pattern recognition receptors of the innate immune system which recognize viral nucleic acids. Nucleic acids are, however, also integral components of the host cell. This implies that cells must be equipped with efficient means to avoid inappropriate recognition of self-nucleic acids and to prevent detrimental immune activation. Combining genetics, molecular and cell biology, we aim to dissect disease mechanisms underlying the phenotypic expression of autoinflammation and autoimmunity.
Future Projects and Goals
- To identify genes causing monogenic and multifactorial autoinflammatory and autoimmune diseases in humans and to unravel their contribution to disease pathogenesis.
- To understand the role of the innate immune system in mechanisms of immune defense and tolerance.
- To translate basic science knowledge into clinically relevant concepts.
Methodological and Technical Expertise
- molecular and cell biology
- protein biochemistry/recombinant protein expression
- confocal microscopy
- flow cytometry
- disease modeling using iPSCs