The Paludan Laboratory explores how the innate immune system detects and controls viral infections, with emphasis on the brain. We aim to uncover how restriction factors, innate sensors, and neuroimmune interactions determine whether immune activation leads to protection or pathology. By defining these mechanisms, we seek to guide new strategies that enhance antiviral defense while limiting damaging inflammation in the nervous system and other tissues.

 

1) Innate sensing of viruses and immune signaling

We seek to understand how host cells detect invading viruses and translate these encounters into protective immune programs. Our work explores the molecular mechanisms by which restriction factors control viral replication and how virus-sensing innate immune receptors coordinate antiviral and inflammatory signaling. We are particularly interested in how these systems integrate spatial and temporal cues, interact with cellular stress pathways, and are regulated to balance defense with tissue integrity. By dissecting these processes, we aim to reveal principles that can be harnessed to fine-tune innate immune responses for therapeutic benefit.

 

2) Neuroimmunology and inflammation

We are fascinated by how the immune system functions within the unique environment of the central nervous system. Our research investigates how neurons, astrocytes, and microglia detect infection, communicate through cytokine and interferon networks, and maintain the balance between antiviral protection and neuroinflammation. We aim to define the molecular logic that governs this balance, and to uncover how chronic or dysregulated immune activity contributes to neurological disease. Through integrated in vivo and in vitro approaches, we work towards a understanding of innate immunity in the brain from molecule to organ function.

 

3) Infection pathogenesis

We study how viruses interact with host tissues to drive both protective and pathogenic immune responses. By focusing on neurotropic and mucosal infections, we aim to uncover how host–virus interactions shape disease outcome—from efficient viral clearance to immunopathology and persistence. Our goal is to identify the checkpoints at which innate immunity can be redirected to prevent severe disease, promote tissue repair, and restore immune homeostasis. These insights provide a foundation for developing new immunomodulatory strategies against viral infections affecting the brain and beyond.