We are developing the idea that effector mechanisms in autoimmune inflammation involve components of both the adaptive and the innate immune system. We are also exploring whether autoimmune and auto-inflammatory diseases may be using common effector pathways, including: a) extracellular and intracellular immune receptors such as toll like receptors (TLRs) and other danger signal receptors (e.g. NOD-like receptors, STING) that transduce signals via the adaptor molecules, b) immune receptors that participate in the formation of the inflammasome, c) cytokines (such as IFNs, IL-10, IL-33 and IL-21), d) innate immunity pathways such as autophagy and NETosis, and e) metabolic pathways such as mitochondrial function and oxidative phosphorylation.
We are interested in the regulation of genes involved in T- and B-cell function and how epigenetic factors (micro-RNAs, histone modifications) may contribute to pathogenesis of autoimmune disorders.
We focus on the role of immune cells (dendritic cells, Tregs cells, plasmacytoid DCs (pDCs), myeloid derived suppressor cells MDSCs) in controlling immune tolerance in the context of human immune mediated diseases.
At the translational level, we use novel biologic therapies targeting specific components of the immune response to characterize their importance in the disease and in selected aspects. Based on preliminary clinical and laboratory information, we are promoting the notion that quantitative and qualitative characteristics of the response of tissues to the inflammatory attack (kidneys, joints) may contribute to the disease phenotype.