Research Interests

T lymphocytes are cells of our immune system that are necessary to protect from infections. Since they need to tackle many different pathogens, there are different types of T cells. Each T cell type is dedicated to a specific group of pathogens and secretes effector molecules (cytokines) evolved to fight such pathogens (Figure 1). In addition to their anti-pathogenic role, T cells protect us from cancer, while failure to dampen their activity may result in chronic inflammation or autoimmunity (Figure 1).


Figure 1. Types of T cell mediated immunity. There are three types of T cell mediated immunity: type 1, which has evolved to fight intracellular bacterial, viruses and tumors; type 2, which has evolved to fight helminths and parasites; type 3, which has evolved to fight extracellular bacteria and fungi. Each type of immunity is driven by specialized T cell subsets that secrete cytokines specific to the pathogen: type 1 T cells produce interferon(IFN)-γ; type 2 T cells produce interleukin(IL)-4 and IL-13; type 3 T cells produce IL-17 and IL-22. The genes coding these cytokines are driven by the indicated transcription factors (Tbet, GATA3, RORγt) for each type of T cell; these transcription factors additionally define many characteristics of T cell biology (e.g. proliferation, survival, migration). T cells that express the transcription factor FoxP3 are regulatory and their main role is to suppress T cell responses. Failure to regulate T cell immunity can result in serious chronic inflammatory diseases and autoimmunity.

Our group is interested in T cells that produce the cytokine interleukin(IL)-17 and are termed either type-17 or type-3. IL-17-producing T cells are required to protect from infections like fungi and extracellular bacteria but have been shown to be pathogenic in many chronic inflammatory diseases such as multiple sclerosis or psoriasis (Figure 2). Understanding how these T cells develop and function will give us a tool in manipulating them for therapeutic purposes. We are particularly interested in CD4+ T helper-17 (Th17) and gamma delta (γδ) T-17 (γδT17) cells.


Figure 2. IL-17-producing γδ T (γδT17) and CD4+ T-helper (Th17) cells. γδT17 cells are exported from the thymus after birth fully functional and do not require antigenic stimulation. Th17 cells differentiate from naive CD4+ T cells in response to antigen. Both γδT17 and Th17 cells are part of type 3 immune responses against extracellular bacteria and fungi. When dysregulated γδT17 and Th17 mediated responses have been linked with numerous inflammatory diseases including multiple sclerosis, psoriasis, rheumatoid arthritis and IBD. The colored dots indicate our group’s interests which include γδT17 cell development post thymic export, Th17 differentiation, and the function of both cell types in the context of infection and inflammation. We aim to elucidate signaling pathways that regulate each of these biological processes.


Th17 cells are part of the adaptive immune system, and differentiate in response to antigenic stimulation after their naive counterparts leave the thymus – the organ where all T cells develop. In contrast, γδT17 cells are innate – i.e. they do not require TCR-antigen interactions to respond – and acquire most of their effector functions before they leave thymus (Figure 2). At steady-state, both Th17 and γδT17 cells are found mainly at mucosal surfaces, the skin and secondary lymphoid tissues (e.g. lymph nodes), however, during infection and inflammation they can migrate to any organ. The objective of our lab is to elucidate which signaling pathways and molecules regulate the development, differentiation and function of Th17 and γδT17 cells (Figure 2).