/ News, Research
Unveiling CD52 on monocytes: A New Frontier in Combating Immune Dysfunction in Cirrhosis (Bernsmeier Lab)
The Department of Biomedicine (DBM) is pleased to announce an important new study led by Anne Geng, under the supervision of Christine Bernsmeier, in collaboration with researchers at the University Hospital Basel and colleagues in St. Gallen, London, and Birmingham. They investigated the immune dysfunction underlying susceptibility to infection in cirrhosis patients, particularly focusing on the role of monocyte heterogeneity and function at different stages ot the disease.
The study used single-cell RNA sequencing to subset monocyte clusters and revealed changes in their abundance and function between compensated and non-acute decompensated cirrhosis. A key finding was the discovery of CD52 as a critical marker on monocytes, which augmented in early stages of cirrhosis and enhanced monocyte functions such as phagocytosis, cytokine release and migration while reducing T-cell activation. However, during acute decompensation, CD52 was presumably cleaved by elevated phospholipase C, deteriorating monocyte function and correlating with higher infection rates and poorer outcomes. These findings implicate CD52 as a biomarker of innate immune function in liver cirrhosis, which may be a promising target for future immunotherapies to improve infection control and patient prognosis.
We congratulate Anne Geng, Christine Bernsmeier, and their collaborators for this important contribution to the understanding of immune dysfunction in cirrhosis.