Professor Sammy Bedoui

• Key Achievements
• Publications
• Projects
• Research Groups

• Key Achievements

  • Sammy’s research has defined how particular types of T cells protect the host from Salmonella infections, uncovering that these responses are regulated through the stimulation of protein complexes within dendritic cells, the so-called inflammasomes. His work on virus infections has identified how different dendritic cell types contribute to the initiation of virus-specific immunity and has delineated how specific viral fragments augment these responses. Ongoing work interrogates the mechanisms by which T cells ‘help’ dendritic cells in driving immune responses. Overall, Sammy’s work has shed new light into understanding how dendritic cells integrate multiple signals into protective immunity against infections.

  Publications
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  Projects

  • Role of innate signals in inducing protective T cell immunity

    Although it is clear that the innate and the adaptive immune system are inextricably linked, precisely how these two arms of the immune system interact still remains unclear. This project examines how specific pathogen sensing pathways contribute to effective killer T cell responses. Sammy’s group is specifically interested in type I interferons and how these are induced and regulated in dendritic cells through molecules or molecule complexes such as toll-like receptors, STING and inflammasomes.

  • Delineating how CD4 T cells ‘help’ establishing effective killer T cell responses

    Resolution of virus infections relies on the orchestrated activation of dendritic cells (DC), CD4 T cells and killer T cells. We have known for some time that CD4 T cells contribute to killer T cell immunity, but how CD4 T cells, DC and killers interact in vivo is still unclear. Using a model of peripheral virus infection, Sammy’s group found that CD4 T cells contributed to CTL immunity by amplifying the IFN-α/β-induced provision of IL-15 by DC to CTL. Building upon these novel findings, they are currently dissecting the molecular mechanisms.

  • Understanding the interaction between microbiota and T cell immunity

    Development of autoimmune diseases has been linked to disturbances in the microbes that normally colonise our body surfaces. However, precisely how these microorganisms and the resulting stimulation of the immune system impact on T cells still remains elusive. Building on extensive preliminary data available in the lab, this project investigates how the microbiota influences particular cytokine responses that are highly relevant to our understanding of T cell-mediated autoimmune disease, such as type I diabetes.

  • Deciphering the relative contributions of different Dendritic cells to killer T cell responses

    Continuing our endeavor to resolve the role of dendritic cells (DC) in virus infections, this project investigates the relative contributions of different DC subtypes to killer T cell priming and examines the molecular pathways involved (direct versus cross-presentation). Utilising in vivo models that remove the capacity of cells to directly present viral antigen, Sammy’s group found that robust virus-specific killer T cell responses depend on cross-presentation. They are currently delineating the underlying mechanisms.

  Research Groups

  • Bedoui Group

    The Bedoui Lab uses models of viral and bacterial infection to study how the innate and the adaptive immune system interact. Key foci are to understand how innate cells sense pathogens and how this information is integrated into protective adaptive T cell responses.

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    Lab Team

    

    • Dr Paul Whitney

      Research Officer
    • Annabell Bachem

      Research Officer
    • Ms Marie Greyer

      PhD student
    • Ms Elise Gressier

      PhD student
    • Mr Newton Gil Peres

      PhD student
    • Mr Max Chao

      PhD student

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