Lab Header · Kettritz

Kettritz Lab

Nephrology and Inflammatory Vascular Diseases


Autoimmune vasculitidis are inflammatory small-vessel diseases affecting every organ, including the kidneys. Steroids, cytotoxic agents and anti-CD20 antibodies are standard therapies that improved outcome but harbor their own mortality and morbidity issues. Better understanding of disease mechanisms will identify novel treatment strategies.

We are interested in systemic autoimmune vasculitides, particular those featuring anti-neutrophil cytoplasmic autoantibodies (ANCA). We care for an ANCA vasculitis patient cohort at the Charite clinics and explore molecular mechanisms by which ANCA-activated innate immune cells damage the endothelium leading to necrotizing vasculitis in our laboratory at the ECRC.


Group Leader

Prof. Dr. Ralph Kettritz


Scientists, clinical fellows and graduate students

Dr. Adrian Schreiber

Dr. Mira Choi

Dr. Julia Bontscho

Dr. Uwe Jerke

Dr. Astrid Bergmann

Claudia Eulenberg



Prof. Friedrich C. Luft


Technical Assistants

Susanne Rolle

Sylvia Krüger


Research team Kettritz



We study molecular mechanisms by which ANCA activate the ANCA antigen-expressing neutrophils and monocytes and how these activated cells damage the endothelium.

An initial step in the inflammatory cascade is binding of ANCA to their autoantigens on the cell surface of neutrophils and monocytes. Proteinase 3 (PR3) and myeloperoxidase (MPO) are the major ANCA target antigens. In contrast to MPO which is found on all neutrophils, PR3 shows a bimodal surface pattern with low- and high-expressing neutrophil populations. This bimodal pattern results from neutrophil subset-restricted expression of the PR3 receptor CD177 that supports high PR3 amounts on the neutrophil surface. We study genetic and epigenetic mechanisms that are responsible for this clinically relevant bimodal CD177-mediated mPR3 pattern. Moreover, we explore strategies to disrupt the CD177-PR3 complex to reduce PR3-ANCA binding and neutrophil activation.

CD177 provides an example for neutrophil heterogeneity. We study causes and functional consequences of this phenomenon with implications above-and-beyond ANCA vasculitis. For example, CD177 ligands other than PR3 may exist. We will search for such ligands using biological samples from patients with inflammatory diseases.

ANCA bind to and activate the neutrophil and monocyte. Study ANCA-induced responses in these innate immune cells that contribute to vascular inflammation. Moreover, we study neutrophil and monocyte interactions and how these interactions modify inflammation.