Macrophage biology and innate cellular networks in chronic inflammatory diseases

One focus has been to uncover pathways that give rise to  disease-associated  macrophage and osteoclasts in TNF-driven chronic inflammatory processes, such as the role of the DNA Damage Response in granulomatous diseases, arthritis and bone regeneration.

Another focus is to shed light on the innate lymphoid cell-macrophage-parenchymal cell crosstalk that sustains homeostasis and the role of this network in amplifying inflammatory responses and organ damage in autoimmune diseases.

Ongoing projects aim to dissect the role of innate cells and innate cell receptors as homeostatic regulators and mechanistic determinants of tissue damage and regeneration in a broad range of conditions, including  lupus nephritis, CNS lupus, TNF-driven granulomatous ileitis, TNF-induced osteoclastogenesis and bone regeneration, and alveolar homeostasis.

Group leader
Prof. Antigoni Triantafyllopoulou, M.D./Ph.D.

Scientists
Dr. rer. nat. Stylianos-Iasonas Biniaris-Georgallis, M.D. (Junior Clinician Scientist)
Katerina Stergioula, M.D., Ph.D. cand.

PhD. students
Paula Maria Bianchi, M.Sc.
Vajiheh Jafari, M.Sc.
Tejal Karmalkar, M.Sc.
Ana Kasapi, M.Sc.

Medical students
Lea Fabry

Lab Manager
Frauke Schreiber (B.T.A)

Andreas Diefenbach, Mir-Farzin Mashreghi, Anja Hauser, Efstathios Stamatiades, Max Löhning, Andrey Kruglov, Chiara Romagnani, Gerhard Krönke, Eicke Latz, Georg Duda, Eva Schrezenmeier.

Andreas Schlitzer (Bonn), Kevin Thurley (Bonn), Reinhard Voll (Freiburg)

Stipan Jonjic (Croatia), Marco Colonna (US), Martina Molgora (US) Eric Vivier (France), Christoph Schneider (Zürich)