Neutrophils Take on a New Role in Antifungal Defense
Invasive aspergillosis, caused by the fungal pathogen Aspergillus fumigatus, is a major cause of mortality in patients undergoing hematopoietic and solid organ transplantation. Earlier studies established a role for the cytokine interleukin-17A (IL-17A) in A. fumigatus host defense. Werner and colleagues (p. 3966–3977) demonstrate that the immune cell required for clearing A. fumigatus from the lungs, the neutrophil, is an early cellular source of IL-17A. This work demonstrates that IL-17A production in neutrophils isolated from the lungs of infected mice and in peritoneal neutrophils from naïve mice stimulated with A. fumigatus is dependent on recognition of A. fumigatus by the beta-glucan receptor Dectin-1 and on Dectin-1-mediated IL-23 production. This work supports a new understanding for the role of neutrophils in invasive aspergillosis.
Pneumococcus-Infected Monocytes Induce a Mixed Th1/Th17 Response
Recent findings suggest that T helper (Th) cells contribute to acquired immunity to Streptococcus pneumoniae. Olliver and colleagues (p. 4210–4217) study bacterial and host factors involved in the induction of memory Th1 and Th17 responses in the human system using a coculture model of monocytes and CD4+ T cells. In this study, the authors show that purified pneumococcal peptidoglycan triggers both Th1 and Th17 cytokines but that the balance between the two immune effector arms depends on bacterial viability. These findings provide insight that may facilitate the design of pneumococcal vaccines and the development of novel immunomodulatory therapies.
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