The Lymphocyte Cell Biology Unit investigates early stages of the adaptive immune response, in particular the molecular mechanisms that lead to the generation and function of immunological synapses, and their subversion by the lymphotropic retroviruses HIV-1 and HTLV-1.
The infection of an organism by a pathogen (e.g. virus or bacteria) triggers a specific and long lasting immune response, called the adaptive immune response that allows the defense of the organism. T lymphocytes are in the center of adaptive immune responses, since they contribute to their regulation and to the destruction of infected or cancer cells.
T lymphocytes are activated when they detect on the surface of antigen presenting cells the presence of molecular fragments (antigens) derived from pathogens. When a T cell recognizes its specific antigen, it polarizes towards the antigen-presenting cell, generating an organized cell-cell contact named the immunological synapse. Immunological synapses are multitask interfaces that allow the triggering and control of T cell activation, leading to proliferation and differentiation. They also enable T cell effector functions, like polarized secretion of cytokines and of cytotoxic granules.
Our goal is to elucidate how immunological synapses are generated and control T cell functions. We investigate the role of receptors and intracellular signaling molecules, of the actin cytoskeleton and microtubules and of intracellular vesicle traffic, in the formation of immunological synapses and in T cell activation. We also study how retroviruses that infect T lymphocytes, such as the human immunodeficiency virus (HIV-1), or the human T cell leukemia virus (HTLV-1) subvert the mechanisms of generation of immunological synapses in order to modulate T cell responses and to better spread from cell to cell.