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To elucidate mechanisms that control the initiation of inflammatory responses.

Signal integration between different classes of innate receptors allows the specification of inflammatory responses.

The type and purpose of the inflammatory response are context-dependent. During infection, inflammation aims to eliminate the insult and induce protective immunity. In contrast, inflammation incited by sterile tissue injury aims to limit the damage and enable tissue repair. In most cases, the same immune cells (such as macrophages), receptors and signaling pathways control both types of inflammatory responses. How such an overlapping system directs the response that is tailored to specific pathological state remains poorly understood. Addressing this fundamental knowledge gap will unveil targets for the design of therapies against chronic inflammatory diseases without compromising the patient’s antimicrobial defenses. 

Major research objectives

1. How do myeloid cells initiate an inflammatory response? 

Innate immune cells, such as macrophages and dendritic cells are sentinels of tissue homeostasis. Our group investigates how these cells integrate signals from cytokines (which report on infection or tissue injury) with signals from microbial and tissue-damage sensors to direct the most appropriate effector response.  Specifically, we study a novel class of cytokine-regulated surface glycoproteins on macrophages and dendritic cells and their roles in shaping the downstream inflammatory responses.  

2. How is inflammatory signalling deactivated? 

The NLRP3 inflammasome is a critical intracellular sensor of cell and tissue homeostasis that becomes activated in response to pathogen- or tissue-derived danger signals. Activated NLRP3 inflammasome drives the secretion of proinflammatory cytokines IL-1 and IL-18 to initiate the downstream inflammatory responses, while at the same time it induces proinflammatory death of infected and damaged cell. While activation of the NLRP3 inflammasome is beneficial during infections, excessive and uncontrolled NLRP3 activity contributes to the development of several inherited and acquired inflammatory diseases such as Cryopyrin-Associated Periodic Syndromes (CAPS), Gout, Alzheimer’s, Parkinson’s and aging associated inflammation and functional decline. Hence, we study how the NLRP3 pathway activity is ‘turned on and off’ in healthy individuals to be able to harness this knowledge for therapeutic interventions.  


Selected publications