The immune system functions as a network in which immune cells are continuously subjected to various soluble, cellular or pathogenic signals that condition their behavior and fate. These cells are also the main target of HIV-1 and contribute significantly to the dissemination of the virus in the body. Our past research activities have uncovered key signaling pathways involved in converting external signals into an appropriate T cell response, but also has led to a better understanding of how HIV-1 hijacks and disrupts basic cellular pathways to optimize essential steps in the life cycle of the virus in the natural target cells of HIV-1, T cells and macrophages.
The objectives of our team, in line with these previous efforts, are to address new questions on the dynamics of immune cell signaling after chemokine stimulation, activation or retroviral infection, and on the analysis of their consequences on T cell activation and cell-to-cell virus transfer and dissemination in macrophages and dendritic cells.
Thus, we study the signaling pathways and cytoskeleton remodeling triggered in immune cells in response to various stimuli in a physiological, inflammatory, tumor and infectious context. In particular, we analyze the involvement of Rho family GTPases in immune responses. We also study the role of FoxO1, one of the main transcription factors in T cells, in the immune responses, especially antiviral. Finally, we are trying to determine the mechanisms controlling HIV-1 infection of T cells, macrophages and dendritic cells through cell-to-cell transfer of the virus. More recently, a project on SARS-CoV-2, the etiological agent of Covid-19, has also been initiated.

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Clotilde Randriamampita

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