Complement is one of the most ancient defense systems of our body that is part of innate immunity and is formed by soluble proteins, membrane integrated molecules and receptors. Complement proteins play a crucial role in several diseases and modify the activation and function of inflammatory cells, such as neutrophil granulocytes.

Genetic analyses revealed that the competition between complement factor H and the factor H-related FHR proteins on various ligands (e.g., on surfaces covered by extracellular matrix components) play important roles in inflammation, as these molecules modify the activation of complement and immune cells. The role of the interaction between complement and extracellular matrix molecules in various inflammatory diseases (e.g., glomerulonephritis, age-related macular degeneration, rheumatoid arthritis) is known, but the detailed mechanism of these pathological processes is poorly explored.

The aim of our project is to unravel which extracellular matrix components bind factor H and FHR proteins, and to examine the effect of these interactions on neutrophil activation. To this end, ELISA , microarray and microfluidic techniques will be applied.

Our research groups possess state of the art techniques in the field of complement proteins and cell binding measurements. Combination of these methods enables examination of interactions between complement, extracellular matrix components and immune cells from minimal volume of serum or whole blood, which will facilitate the understanding of the pathomechanism of inflammatory diseases.

Zoltán Prohászka - Mihály Józsi - Krisztián Papp


Report I. 2016. september

Report II. 2016. november

Report III. 2017. january