Toxoplasma gondii est capable de moduler les différentes voies de l'apoptose afin de se disséminer et de persister dans les cellules du système nerveux central. ![]() Etude de l'apoptose des cellules du système nerveux central humain infectées par Toxoplasma gondii This immune axis thus regulates the development of a protective host response to respiratory bacterial infections. Our work revealed the cellular and molecular dynamic events leading to cdT17 cell activation, and highlighted for the first time the existence of a fully functional NLRP3 inflammasome in lung neutrophils. Interestingly, this mechanism can be translated to human neutrophils. Elaborately, it relies on (i) alveolar macrophagesecreted TNF-a for priming and (ii) subsequent exposure to bacterial pneumolysin for activation. ![]() In vivo activation of the NLRP3 inflammasome in neutrophils required both host-derived and bacterial-derived signals. Using a model of invasive pneumococcal disease, we highlighted an unexpected key role for neutrophils as accessory cells in innate interleukin (IL)-17A production by lung resident Vg6Vd1+ Tcells via nucleotide-binding oligomerization domain receptor, pyrin-containing 3 (NLRP3) inflammasome-dependent IL-1b secretion. Traditionally regarded as simple foot soldiers of the innate immune response limited to the eradication of pathogens, neutrophils recently emerged as more complex cells endowed with a set of immunoregulatory functions.
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