Inflammatory and Cell Death Signalling in Diabetes
Group Leader, Prof Alessandra K. Cardozo
The Inflammatory and Cell Death Signalling in Diabetes group combines cell biology, immunology, genomics and proteomics to investigate how inflammatory, metabolic and cell-death pathways drive pancreatic β-cell dysfunction and destruction in type 1 diabetes.
Research Interests
Prof Alessandra K. Cardozo pioneered transcriptomic profiling in primary β-cells. Her early findings helped reshape the type 1 diabetes field by demonstrating that β-cells are not passive victims of immune attack. Instead, they actively sense inflammatory signals, communicate with immune cells and contribute to the amplification of islet inflammation. Her research also identified NF-κB as a central regulator of these inflammatory and pro-apoptotic responses and uncovered important interactions between cytokine signalling, endoplasmic reticulum stress and mitochondrial apoptosis.
Building on these discoveries, her group investigates the molecular checkpoints determining whether β-cells survive or die in an inflammatory environment, including apoptosis, necroptosis and other regulated cell-death pathways. A major current focus is immunometabolism: understanding how metabolic reprogramming sustains autoreactive immune-cell activation and function. The ultimate goal is to restrain pathogenic immunity without causing broad immunosuppression while preserving functional β-cell mass.
The group also applies its expertise in inflammatory and cell-death signalling to other chronic inflammatory disorders. In collaboration with Dr Benjamin Bondue, interventional pulmonologist and expert in interstitial lung diseases at Brussels University Hospital (HUB), the team investigates inflammatory mechanisms contributing to idiopathic pulmonary fibrosis (IPF). This work aims to identify molecular mechanisms that sustain inflammation and promote progressive tissue remodelling in the fibrotic lung.
Current research topics include:
Metabolic regulation of autoreactive T-cell responses
Lactate metabolism and monocarboxylate transport
β-cell–immune-cell communication
Regulated β-cell death
Immunometabolic strategies to preserve β-cell function
Inflammatory mechanisms driving IPF
Prof Alessandra K. Cardozo, PhD
Alessandra K. Cardozo obtained her Master’s degree in 1999 and PhD in 2003 from the Vrije Universiteit Brussel, Belgium. In 2006, she was appointed Research Associate (Chercheuse qualifiée) of the F.R.S.–FNRS and established her research group at the Faculty of Medicine of the Université libre de Bruxelles (ULB). She joined the ULB academic staff in 2015 and was appointed Professor in 2024.
Prof. Cardozo is a Senior Principal Investigator at the Signal Transduction and Metabolism Laboratory, where she leads the Inflammatory and Cell Death Signalling in Diabetes group. Her expertise in β-cell inflammation, regulated cell death and immunometabolism complements the laboratory’s research on β-cell biology, metabolic signalling and diabetes. The groups collaborate closely to investigate the crosstalk between pancreatic β-cells and immune cells and the molecular mechanisms driving β-cell dysfunction and loss in diabetes.
Email: Alessandra.Kupper.Cardozo [at] ulb.ac.be
Honours & Awards
2025 | Breakthrough T1D Strategic Research Agreement
2024 | Université libre de Bruxelles (ULB) Promotion Tenured Professor
2018 | FNRS / Research Foundation Flanders (FWO) Excellence of Science (EOS) Grant
2009 | Sanofi-Aventis Award in Diabetes
2006 | Fonds de la Recherche Scientifique (FNRS) Tenured Research Associate / Chercheuse qualifiée
2005 | European Association for the Study of Diabetes (EASD) / Amylin Pharmaceuticals Paul Langerhans Research Award for Research on the Physiology and Pathophysiology of β-cells
2004 | Juvenile Diabetes Research Foundation (JDRF) International Postdoctoral Fellowship
2004 | Victor Lange Prize for Diabetes Research in Belgium
2000 | Belgian Endocrine Society (BES) Young Investigator Award
1998 | Vrije Universiteit Brussel (VUB) Advice Council for Development Cooperation (VUBAROS) Scholarship, Master in Medical and Pharmaceutical Research
Selected Publications
Takiishi T, Xiao P, Franchimont M, Gilglioni EH, Arroba EN, Gurzov EN, Bertrand MJ, Cardozo AK. Inhibition of RIPK1 kinase does not affect diabetes development: β-Cells survive RIPK1 activation. Molecular Metabolism 69:101681, 2023
Lavis P, Morra S, Orte Cano C, Albayrak N, Corbière V, Olislagers V, Dauby N, Del Marmol V, Marchant A, Decaestecker C, Mascart F, De Vos N, Van de Borne P, Salmon I, Remmelink M, Parmentier M, Cardozo AK, Bondue B. Chemerin plasma levels are increased in COVID-19 patients and are an independent risk factor of mortality. Front Immunol 13:941663, 2022
Xiao P, Takiishi T, Violato NM, Licata G, Dotta F, Sebastiani G, Marselli L, Singh SP, Sze M, Van Loo G, Dejardin E, Gurzov EN, Cardozo AK.NF-κB-inducing kinase (NIK) is activated in pancreatic β-cells but does not contribute to the development of diabetes. Cell Death Dis 13(5):476, 2022
Tiezzi M, Morra S, Seminerio J, Van Muylem A, Godefroid A, Law-Weng-Sam N, Van Praet A, Corbière V, Orte Cano C, Karimi S, Del Marmol V, Bondue B, Benjelloun M, Lavis P, Mascart F, van de Borne P, Cardozo AK. SP-D and CC-16 Pneumoproteins' Kinetics and Their Predictive Role During SARS-CoV-2 Infection. Front Med (Lausanne) 8:761299, 2022.
Meyerovich K, Violato NM, Fukaya M, Dirix V, Pachera N, Marselli L, Marchetti P, Strasser A, Eizirik DL, Cardozo AK. MCL-1 is key anti-apoptotic protein in human and rodent pancreatic β-cells. Diabetes 66:2446-2458, 2017
Fukaya M, Brorsson CA, Catrysse L , Delaroche D, Vanzela EC, Meyerovich K, Ortis F, Beyaert R, Nielsen LB, Andersen ML, Mortensen HB, Pociot F, van Loo G, Størling J, Cardozo AK. TNFAIP3/A20 inhibits β-cell apoptosis by multiple mechanisms and predicts residual β-cell function in children newly-diagnosed for type 1 diabetes. Molecular Endocrinology 30:48-61, 2016
Meyerovich K, Fukaya M, Terra LF, Ortis F, Eizirik DL, Cardozo AK. The non-canonical NF-κB pathway is induced by cytokines in pancreatic β-cells and contributes to cell death and pro-inflammatory responses. Diabetologia 59:512-21, 2016
Allagnat F, Fukaya M, Nogueira TC, Welsh N, Marselli L, Marchetti P, Eizirik DL, Cardozo AK. C/EBP Homologous Protein (CHOP) Contributes to Cytokine-induced Pro-Inflammatory Responses and Apoptosis in Beta Cells. Cell Death Diff 19:1836-1846, 2012
Allagnat F, Cunha D, Moore F, Vanderwinden JM, Eizirik DL, Cardozo AK. Mcl-1 degradation by pro-inflammatory cytokines and palmitate is an early and major event for beta cell apoptosis. Cell Death Differ 18:328-37, 2011
Allagnat F, Christulia F, Ortis F, Pirot P, Lortz S, Lenzen S, Eizirik DL, Cardozo AK. Sustained expression of spliced XBP1 induces pancreatic beta-cell dysfunction and apoptosis. Diabetologia 53:1120-30, 2010 (Cover page of this issue)
Pirot P, Ortis F, Yanjun M, Hendershot L, Eizirik DL, Cardozo AK. Transcriptional regulation of the endoplasmic reticulum (ER) stress gene CHOP in pancreatic β-cells. Diabetes 56:1069-1077, 2007
Cardozo AK, Ortis F, Storling J, Feng Y-M, Rasschaert J, Tonnesen M, Van Eylen F, Mandrup-Poulsen T, Herchuelz A, Eizirik DL. Cytokines downregulate the sarcoendoplasmic-reticulum pump Ca2+-ATPase (SERCA)2b and deplete endoplasmic reticulum (ER)-Ca2+ leading to induction of ER-stress in pancreatic β-cells. Diabetes 54:452-461, 2005
Cardozo AK, Proost P, Gysemans C, Chen MC, Mathieu C, Eizirik DL. IL-1β and IFN-γ induce the expression of diverse chemokines and IL-15 in human and rat pancreatic islet cells, and in islets from pre-diabetic NOD mice. Diabetologia 46:255-266, 2003
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