Myeloid cells are highly plastic cells endowed with an ever-growing list of functions in numerous organs. Moreover, they are pivotal in innate immunity and probably represent the most ancient form of cellular immunity against pathogens and tumor cells.
Our general goal is to decipher the molecular mechanisms involved in the regulation of the interplay between the myeloid cells, viruses and tumors. The lab currently focuses on the following questions taking HIV as a virus model targeting myeloid cells.
How do myeloid cells sense viruses, and how this sensing is regulated?
How viruses can replicate in myeloid cells despite numerous cellular defenses and the response they elicit?
How tumor and myeloid cells impact on each other?
Our research is centered around 2 axes:
1) We analyze how HIV interacts with primary macrophages and dendritic cell subsets. We focus on the anti-viral innate responses and on cell biology aspects of the viral life cycle in these different cell subsets. Such studies not only bring knowledge on HIV infection but also reveal new regulation levels of the innate system. Figures 1 and 2.
2) We have developed models to study, in 3D and in real time, the interplay between myeloid and tumor cells but also with cytotoxic T cells. In this context, we are analyzing immunosuppressive myeloid cells and are developing ways to manipulate them to enhance the anti-tumor immune response for therapeutic purpose. Figure 3.
Figure 1 (left): Immunofluorescence by confocal microscopy of macrophages infected by HIV-1. Nucleus (violet), actin (light blue) tubulin (red), Gag (green)
Figure 2 (right): Live imaging by confocal microscopy of human primary macrophages infected by HIV-1 (in green) and transduced by Life-act cherry.
