The Role of CD177 for the Function of Human Neutrophil Granulocytes

Time
4:00 PM, October 15, 2026 (Beijing)
10:00 AM, October 15, 2026 (Berlin)

Zoom Meeting Link:
 https://us06web.zoom.us/j/84509378668?pwd=032uGWLNcpR99L7JIJHiAtXFY44oMq.1
Meeting ID: 845 0937 8668
Passcode: 792734
Contact Us
Email: mcjournal@sciexplor.com
Speaker
Prof. Matthias Gunzer
Institute for Experimental Immunology and Imaging, University Hospital, University of Duisburg-Essen, Essen, Germany.
1990-1992: Biology studies at the Julius-Maximilians-University in Würzburg. 1992–1995: Studied biochemistry at the University of Witten/Herdecke; completed diploma in 1995 at the Institute of Immunology.
1996–1999: Ph.D. at the Institute of Immunology, University of Witten/Herdecke.
1999–2003: Postdoctoral researcher/scientific assistant at the University Skin Clinic Münster.
2003: Head of the "Immuno-Dynamics" junior research group at the Helmholtz Centre for Infection Research in Braunschweig; habilitation in May 2007.
Since 2011: W3 Professor and Founding Director of the Institute for Experimental Immunology and Imaging at the University of Duisburg-Essen and University Hospital Essen. Also leads research at ISAS (Leibniz-Institut für Analytische Wissenschaften).
Research Focus:
- Immuno-dynamics: Real-time analysis of immune cell behavior and migration in vivo using advanced optical imaging and microscopy.
- Neutrophils: Biology of murine and human neutrophils in infection, inflammation, and cancer.
Introduction
CD177 is considered the human analog of murine Ly6G. It´s function is associated with but not limited to trans endothelial migration. The majority of humans does express the molecule, but a sizeable fraction of the population (e.g., ~5% of individuals in Germany) is CD177-deficient without obvious associated health issues. Also, in humans principally expressing the molecule only a fraction of circulating neutrophils is actually CD177+. It has been hypothesized, that initially CD177- neutrophils will ultimately become CD177+ after activation and that both, CD177+ and CD177- cells, are functionally identical. We have investigated this hypothesis in detail and can demonstrate, that the assumptions are wrong. First, CD177+ and CD177- neutrophils are molecularly and functionally very different and second, CD177- cells form a stable neutrophil population in humans, that never expresses the molecule. In my talk I will showcase the evidence supporting our fundings and how this relates to the outcome of human disease.