![]() ![]() ![]() Ce processus est mal décrit chez l'homme. 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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