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The lab focuses on the regulatory networks between the complement system and other parts of innate immunity and the impact of such interactions on the development of adaptive immune responses. A particular focus is on the anaphylatoxins (AT) C3a and C5a, and their corresponding G-Protein-coupled receptors. The ATs are prototypic pro-inflammatory mediators generated after proteolytic cleavage of C3 and C5 in response to complement activation. ATs are also generated locally within tissues by pathogen-, cell-, or contact system-derived proteases which is important for their pleiotropic biologic effects beyond inflammation. ATs can activate cells of myeloid origin such as granulocytes, monocytes, macrophages, dendritic cells and mast cells, among others, through ligation of three distinct receptors, i.e. the C3a receptor (C3aR), the C5a receptor (C5aR) and the C5aR-like receptor 2 (C5L2).
During the past 10 years it became increasingly clear that ATs exert important regulatory functions beyond their critical roles as mediators of acute and chronic inflammation. In fact, ATs regulate cell apoptosis, tissue regeneration, tissue fibrosis, lipid metabolism as well as innate and adaptive immune responses through their impact on antigen-presenting cells and T cells. Such regulatory functions of ATs and their receptors play important roles in the pathogenesis of allergy, autoimmunity, neurodegenerative diseases, cancer, systemic infection (sepsis) and infections with intracellular pathogens. At present, the laboratory is focusing on the following four projects:
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| Last Updated ( Dienstag, 20. April 2010) |
