Présentation
Mucosal homeostasis requires a delicate equilibrium between immune mechanisms and commensal microorganisms that impacts on the development and maintenance of critical physiological processes including digestion, metabolism or host defense. Several infectious or inflammatory disorders have been associated with dysregulated intestinal homeostasis. The immune system, and notably the innate compartment, plays an essential role in the regulation of host-microbe interactions, but several aspects of this immunological relationship remain unclear.
Recently, additional innate lymphocytes have been discovered named innate lymphoid cells (ILCs) in both humans and mice (1-8). ILCs are early effectors of immunity and provide a means to rapidly respond to infection or inflammation, and are distinguished from T and B cells of the adaptive immune response. Three groups of ILCs are now described: ILC1, ILC2 and ILC3. ILC1 consists of NK cells and other interferon-g producing innate lymphocytes characterized by expression of the transcription factors T-bet and/Eomes. ILC2 secrete ‘TH2-like’ cytokines under the control of the transcription factors GATA-3 and RORa. ILC3 includes several phenotypically distinct cells that express and require the transcription factor RORgt in order to produce notably the cytokines IL-17 and IL-22.
The ILC subsets have been implicated in a wide range of physiological processes including tissue homeostasis and repair, immune defense or development of lymphoid organs. We study ILCs development from hematopoietic precursors using mouse models. Our goal is to understand how ILCs differentiate and function in the context of infection and inflammation. (9-18). These mouse based studies are fundamental in nature, but may provide new insights into the ILC biology that could be applicable to human disease states.
References
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