Maschalidi Lab

Phagocytosis in Inflammation and Tissue Repair

Our goal is to uncover the molecular and cellular mechanisms that govern phagocytosis and to define its role in tissue repair and inflammation.

We aim to map phagocytosis in its native environment by examining the dynamic transcriptomic, interactomic, and epigenomic changes that occur as cells engulf infectious cargo or dying cells—including those undergoing therapy‑induced death in cancer—and within the surrounding tissue.

A central focus of our work is to develop innovative therapeutic strategies that target the phagocytic machinery to improve chronic iflammatory conditions associated with defective phagocytosis, such as diabetes‑related complications, aging and age‑associated diseases, autoimmune disorders and responses to cancer therapy.

By using cutting-edge technologies (single-cell and spatial multi-omics analyses), sophisticated genetic mouse models and microphysiological experimental models for implementing human diseases, we aim to unveil new layers of regulation in both healthy and diseased tissues and to open the door to innovative treatments that restore proper phagocytosis and promote tissue repair.

 

PROJECTS

 


Project description

This project investigates how enhancing efferocytosis—the clearance of apoptotic cells by phagocytes—can improve skin injury repair and accelerate wound closure. Efficient removal of dying cells is essential for maintaining tissue homeostasis, limiting inflammation, and promoting repair. In the skin, effective clearance of apoptotic cells at wound sites is critical for resolving inflammation and restoring the barrier, a process that is often impaired in chronic wounds such as those associated with diabetes or in excessive healing responses that lead to fibrosis. 

The project will develop tools to enhance efferocytosis in vivo, using advanced techniques and genetic mouse models to systematically examine the impact of boosting this process during skin repair and subsequent inflammatory challenges. It will also explore whether prior phagocytic activity induces lasting changes in phagocytes and neighboring cells—an “efferocytic memory”—that influences responses to future injury. 

Ultimately, this work aims to provide fundamental insight into the mechanisms of efferocytosis and its potential as a therapeutic strategy for improving cutaneous wound healing. 

 

Principal Investigator: Sophia Maschalidi

Start date: 2024

Funded under: LEO Foundation

Grant category: Research Grants

Amount: DKK 3,986,871

Link: https://leo-foundation.org/en/grantee/?grant-category=research-grants-in-open-competition&grant-geography=belgium

 


Project description

Several studies have highlighted that targeting or modulating MHC class II antigen presentation can be beneficial for T1D pathology control. This proposal has the potential not only to reveal novel aspects of MHC class II antigen presentation but also to enhance its targeting in unhealthy states associated with autoimmunity.

Principal Investigator: Sophia Maschalidi

Start date: 2026

Funded under: EFSD and Lilly European Diabetes Research Programme 

Grant agreement ID: EFSD08-EL25-1376-SM 

DOI: (link to the project): not yet available

 

TEAM

 


Group Leader

Sophia Maschalidi is a Principal Investigator at NIMSB, where she explores the molecular and cellular biology of phagocytosis. Her work focuses on how effective cell clearance drives tissue repair, regulates inflammation, and protects tissues from damage. A key part of her work involves examining cell clearance directly in its native environment by profiling the dynamic transcriptomic, interactomic, and epigenomic landscapes of phagocytes and their neighboring cells.

Sophia completed her studies in Molecular Biology and Genetics in Greece before moving to Paris, where she conducted her doctoral research at the Curie Institute and earned her PhD in Immunology from the University of Paris Descartes. She then joined the laboratories of Geneviève de Saint Basile and Alain Fischer at the Imagine Institute, where she developed a new murine model and a novel therapeutic strategy to study Hemophagocytic Lymphohistiocytic (HLH) syndrome, a severe and life‑threatening immune disorder.

After receiving a prestigious Marie Curie Postdoctoral Fellowship, she joined the lab of Professor Kodi Ravichandran at the VIB‑UGent Center for Inflammation Research. There, she expanded her work on phagocytosis, identifying dendritic cells as key regulators of efferocytosis in the skin and opening new possibilities for improving the treatment of chronic cutaneous wounds.

Since 2023, Sophia has led the Phagocytosis and Tissue Repair Lab at the VIB Center for Inflammation Research and serves as an Assistant Professor in the Department of Biomedical Molecular Biology at Ghent University. Her research has resulted in highly cited publications (≈3000 citations; H‑index 19, Google Scholar), appearances in high‑impact journals, patent applications, and numerous invited talks and featured profiles.

 

                

 


Postdoctoral Fellow 

Paulo Francisco Veiga Bizerra is a researcher in Biological Sciences with expertise in biochemistry, metabolism, and molecular biology. He earned his degree in Animal Science and his Master’s in Animal Science and Technology from São Paulo State University (UNESP), followed by a PhD in Biological Sciences from the State University of Maringá (UEM). During his doctoral studies, he uncovered how impairments in mitochondrial bioenergetics contribute to the acute hepatotoxic effects of the antidepressant clomipramine.

As part of a sandwich PhD program at the Tytgat Institute, University of Amsterdam, Paulo investigated liver immune cells and the signaling pathways of Soluble Adenylyl Cyclase (sAC). His work demonstrated that canonical transmembrane adenylyl cyclase–cAMP–PKA signaling promotes glycogenolysis, while non‑canonical sAC–cAMP–Epac1 signaling suppresses it.

After completing his PhD, Paulo served as a temporary lecturer in Biochemistry at UNESP and pursued postdoctoral research in neurobiology at the University of Campinas (UNICAMP). He is currently a postdoctoral researcher in Maschalidi lab at Ghent University, where he studies the phagocytic clearance of apoptotic cells for better wound healing during primary skin injury repair and upon secondary assaults.

 

           


Postdoctoral Fellow

Burcu Nur Keçeli graduated with distinction from Boğaziçi University in Istanbul, Turkey, in 2014, earning dual Bachelor of Science degrees in Molecular Biology & Genetics and Chemistry. She then moved to Belgium to pursue her PhD in the Faculty of Bioscience Engineering at Ghent University) under the supervision of Prof. Dr. Danny Geelen. Her doctoral research focused on histone variants in the plant model Arabidopsis thaliana and supported by an EMBO fellowship, she also trained with Dr. Frédéric Berger at the Vienna BioCenter, a leading group in histone and chromatin biology.

During her PhD, Burcu realized her scientific interests extended beyond plant sciences and toward molecular mechanisms in immunology and cell biology. She subsequently joined the research group of Dr. Kodi Ravichandran at the UGent Center for Inflammation Research, where she contributed to projects on apoptotic cell clearance (efferocytosis) by dendritic cells.

It is increasingly recognized that immune cells shape their gene‑expression programs through dynamic regulation of histone composition and post‑translational modifications. Yet, the “histone code” governing phagocyte‑mediated cell clearance remains largely unexplored. Under the supervision of Prof. Dr. Sophia Maschalidi, Burcu’s current research focuses on uncovering the role of histone biology in phagocytes during cell clearance.

 

 


PhD Fellow

Hannah K. L. De Cleene earned her bachelor’s degree in Biochemistry and Biotechnology from Ghent University in 2019. She completed her master’s thesis in the laboratory of Prof. Dr. Martin Guilliams at the VIB-UGent Center for Inflammation Research. She is currently pursuing her PhD at Ghent University under the supervision of Prof. Dr. Kodi Ravichandran and Prof. Dr. Sophia Maschalidi. Her research explores how metabolic regulation shapes antigen presentation and the lysosomal functions of dendritic cells. 

 


MSc Fellow

Liese Devos obtained her bachelor’s degree in Biochemistry and Biotechnology from Ghent University in 2024 and is currently completing her master’s degree in the same field. She is conducting her master’s thesis in the lab of Prof. Dr. Sophia Maschalidi at the VIB Center for Inflammation Research. Her research focuses on how disruptions in lysosome‑related genes influence apoptotic cell clearance mediated by dendritic cells.

In the summer of 2024, Liese completed a three‑week internship in the lab of Prof. Dr. Geert Van Loo at VIB, investigating the role of ATG9A in intestinal inflammation. During the 2024–2025 academic year, she spent a full year on Erasmus exchange at the Universidad Autónoma de Madrid. In the second semester of her exchange, she carried out an additional bachelor research project in the lab of Prof. Dr. Wilfried Meijer at the Centro de Biología Molecular Severo Ochoa, where she studied Bacillus subtilis and its native plasmid pLS20.

 

 

 

SELECTED PUBLICATIONS

 

Sophia Maschalidi*, Parul Mehrotra, Burcu N. Keeli, Hannah K. L. De Cleene, Kim Lecomte, Renée Van der Cruyssen, Pauline Janssen, Jonathan Pinney, Geert van Loo, Dirk Elewaut, Ann Massie, Esther Hoste, Kodi S. Ravichandran* Targeting Slc7a11 improves efferocytosis by dendritic cells and wound healing in diabetes. Nature (2022) (doi:10.1038/s41586-022-04754-6) *Co-corresponding author

 

Parul Mehrotra*, Sophia Maschalidi*, Laura Boeckaerts, Christian Maueröder, Rochelle Tixeira, Jonathan Pinney, Javier Burgoa Cardás, Vladimir Sukhov, Yunus Incik, Christopher Anderson, Bing Hu, Burcu N. Keçeli, Amanda Goncalves, Liesolette Vande Walle,  Nina Van Opdenbosch, Esther Hoste, Umang Jain, Mohamed Lamkanfi, and Kodi S. Ravichandran. Oxylipins and metabolites from pyroptotic cells act as promoters of tissue repair. Nature (2024) (doi:10.1038/s41586-024-07585-9) *Co-first authors

 

Bartosz Wiernicki, Sophia Maschalidi*, Jonathan Pinney, Sandy Adjemian, Tom Vanden Berghe, Kodi Ravichandran, Peter Vandenabeele.* Cancer cells dying from ferroptosis impede dendritic cell anti-tumor immunity. Nature Communications (2022) (doi:10.1038/s41467-022-31218-2)  *jointly supervised the work

 

Maschalidi S, Nunes P, Nascimento C, Salent I, Lannoy V, Garfa-Traore M, Cagnard N, Sepulveda FE, Vargas P, Lennon-Duménil AM, van-Endert P, Capiod T, Darasse-Jèze G, Demaurex N, Manoury B. UNC93B1 associates with the calcium sensor STIM1 for efficient antigen cross-presentation in dendritic cells. Nature Communications (2017) (doi: 10.1038/s41467-017-01601-5)

 

Maschalidi S, Sepulveda FE, Garrigue A, Fischer A, de Saint Basile G. Therapeutic effect of JAK1/2 blockade on the manifestations of hemophagocytic lymphohistiocytosis in mice.  Blood (2016) (doi: 10.1182/blood-2016-02-700013)