Deciphering the neurotoxic mechanisms of chitinase 3-like 1 (CHI3L1) in progressive multiple sclerosis and identification of therapeutic compounds blocking its pathogenic effects VHIR is seeking an outstanding and highly motivated postdoctoral researcher to apply for a Marie Sklodowska-Curie Postdoctoral Fellowship and join the Clinical Neuroimmunology Research Group.

Marie Skłodowska-Curie Actions – Postdoctoral Fellowships (MSCA-PF) The Marie Skłodowska-Curie Postdoctoral Fellowships (MSCA-PF) are part of the Horizon Europe programme and support postdoctoral researchers in developing an original research and innovation project through international mobility. The programme aims to strengthen researchers’ careers through excellent science, international collaboration and interdisciplinary experience, while fostering integration in both academic and non-academic environments.

The MSCA-PF call is highly competitive and represents an excellent opportunity to attract international talent and support researchers in consolidating their scientific careers through an ambitious mobility-based fellowship. The 2026 call closes on 09/09/2026 (17:00 Brussels time). For candidates applying to a European Postdoctoral Fellowship, the fellowship duration is from 12 to 24 months .

Full eligibility details: MSCA Postdoctoral Fellowships 2026 Background Progressive forms of multiple sclerosis (MS) are characterised by chronic neurodegeneration leading to irreversible neurological disability. Current therapeutic options for progressive MS remain limited and only partially effective, highlighting the urgent need for neuroprotective strategies targeting mechanisms of neuronal damage.

Our group identified chitinase 3-like 1 (CHI3L1) as one of the most important prognostic biomarkers associated with disease progression and long-term disability in MS patients. Additional studies performed by our group demonstrated that CHI3L1 exerts direct neurotoxic effects in both murine neurons and human neurons differentiated from induced pluripotent stem cells (iPSCs) derived from MS patients. These findings suggest that CHI3L1 is not only a biomarker of disease progression but also a potential therapeutic target.

The project aims to investigate the molecular mechanisms underlying CHI3L1-mediated neurotoxicity in human neuronal models and to identify compounds capable of neutralising its pathogenic effects. The work will combine stem cell-derived neuronal cultures, molecular and cellular biology, advanced imaging, transcriptomic and proteomic approaches, and drug screening strategies.

This research has strong translational potential, as the identification of compounds blocking CHI3L1 activity may open the door to future clinical trials in patients with progressive MS. Objective Main objectives of the project: To identify intracellular mediators and signalling pathways involved in CHI3L1-induced neuronal toxicity. To identify neuronal receptors mediating the pathogenic effects of CHI3L1. To generate and characterise human iPSC-derived neuronal models.

To identify approved drugs and/or small molecules capable of blocking CHI3L1 activity or preventing its binding to neuronal receptors. To validate candidate compounds in human neuronal cultures as potential therapeutic strategies for progressive MS. Our Group The Clinical Neuroimmunology group at VHIR is dedicated to translational clinical-basic research in MS, with a particular focus on neurodegeneration, biomarkers, neuroinflammation, and the development of innovative therapeutic strategies for progressive forms of the disease.

The group has strong expertise in: Human iPSC generation and differentiation. Neuronal and glial cell cultures. Advanced molecular and imaging techniques. Biomarker discovery. Translational multiple sclerosis research. Main responsibilities and duties: Collaborate with experts in stem cell biology and neuronal differentiation, proteomics and mass spectrometry, bioinformatics and systems biology, drug discovery and virtual screening, as well as neuroimmunology and progressive MS.