Contact information

Dr. rer. nat. Alessandro Annibaldi

Laboratory of Cell Death, Inflammation and Immunity

CMMC - Center for Molecular Medicine Cologne

University of Cologne

Robert-Koch-Straße 21

50931 Cologne


Academic education

2007 - 2012 PhD studies, University of Lausanne, Switzerland
2000 - 2006 Undergraduate student in Biology at University of Rome “La Sapienza”, Italy


Scientific degrees

02/2012 PhD in Life Science, Department of Physiology, University of Lausanne (UNIL), Switzerland
2009 - 2006 Laurea (eq. Diploma) in Molecular Biology, University of Rome “La Sapienza”, Italy


Scientific career

2019 - present Junior Research Group Leader at Center for Molecular Medicine (CMMC), University Hospital Cologne, Germany
2018 - 2019 Early Career Researcher at Barts Cancer Institute, Queen Mary University of London, UK
2012 - 2018 Postdoctoral fellow at the Institute of Cancer Research (ICR), London, UK (group of Pr. Pascal Meier)


Honors/ Awards/ Memberships

2017 Dean’s Award (£5000). Competitive pump priming award by the Institute of Cancer Research, “Pathway to Independence” program
2015 Advanced Mobility Postdoc Fellowship awarded by the Swiss National Science Foundation (P300P3_147867)
2012 Early Mobility Postdoc Fellowship awarded by the Swiss National Science Foundation (PBLAP3_142759)
2004 Leonardo da Vinci fellowship, awarded by the University of Rome “La Sapienza”



  • Cleavage of cFLIP restrains cell death during viral infection and tissue injury and favors tissue repair

    Cell death coordinates repair programs following pathogen attack and tissue injury. However, aberrant cell death can interfere with such programs and cause organ failure. Cellular FLICE-like inhibitory protein (cFLIP) is a crucial regulator of cell death and a substrate of Caspase-8. However, the…

  • The importance of murine phospho-MLKL-S345 in situ detection for necroptosis assessment in vivo

    Necroptosis is a caspase-independent modality of cell death implicated in many inflammatory pathologies. The execution of this pathway requires the formation of a cytosolic platform that comprises RIPK1 and RIPK3 which, in turn, mediates the phosphorylation of the pseudokinase MLKL (S345 in mouse).…

  • MLKL post-translational modifications: road signs to infection, inflammation and unknown destinations

    Necroptosis is a caspase-independent modality of cell death that requires the activation of the executioner MLKL. In the last ten years the field gained a substantial amount of evidence regarding its involvement in host response to pathogens, TNF-induced inflammatory diseases as well as pathogen…

  • Cell Death-Related Ubiquitin Modifications in Inflammatory Syndromes: From Mice to Men

    Aberrant cell death can cause inflammation and inflammation-related diseases. While the link between cell death and inflammation has been widely established in mouse models, evidence supporting a role for cell death in the onset of inflammatory and autoimmune diseases in patients is still missing.…

  • Chemotherapy Induces Tumor-Associated Macrophages that Aid Adaptive Immune Responses in Ovarian Cancer

    Neoadjuvant chemotherapy (NACT) may stimulate anticancer adaptive immune responses in high-grade serous ovarian cancer (HGSOC), but little is known about effects on innate immunity. Using omental biopsies from HGSOC, and omental tumors from orthotopic mouse HGSOC models that replicate the human…

  • Death Receptors and Their Ligands in Inflammatory Disease and Cancer

    On binding to their cognate ligands, death receptors can initiate a cascade of events that can result in two distinct outcomes: gene expression and cell death. The study of three different death receptor-ligand systems, the tumor necrosis factor (TNF)-TNF receptor 1 (TNFR1), the CD95L-CD95, and the…

  • LUBAC determines chemotherapy resistance in squamous cell lung cancer

    Lung squamous cell carcinoma (LSCC) and adenocarcinoma (LADC) are the most common lung cancer subtypes. Molecular targeted treatments have improved LADC patient survival but are largely ineffective in LSCC. The tumor suppressor FBW7 is commonly mutated or down-regulated in human LSCC, and oncogenic…

  • RIPK1 and Caspase-8 Ensure Chromosome Stability Independently of Their Role in Cell Death and Inflammation

    Receptor-interacting protein kinase (RIPK) 1 functions as a key mediator of tissue homeostasis via formation of Caspase-8 activating ripoptosome complexes, positively and negatively regulating apoptosis, necroptosis, and inflammation. Here, we report an unanticipated cell-death- and…