Publication: Microbe capture by splenic macrophages triggers sepsis via T cell-death-dependent neutrophil lifespan shortening
Microbe capture by splenic macrophages triggers sepsis via T cell-death-dependent neutrophil lifespan shortening
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Ioannou, M., Hoving, D., Aramburu, I. V., Temkin, M. I., De Vasconcelos, N. M., Tsourouktsoglou, T.-D., Wang, Q., Boeing, S., Goldstone, R., Vernardis, S., Demichev, V., Ralser, M., David, S., Stahl, K., Bode, C., & Papayannopoulos, V. (2022). Microbe capture by splenic macrophages triggers sepsis via T cell-death-dependent neutrophil lifespan shortening. Nature Communications, 13(1), 4658. https://doi.org/10.1038/s41467-022-32320-1
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The mechanisms linking systemic infection to hyperinflammation and immune dysfunction in sepsis are poorly understood. Extracellular histones promote sepsis pathology, but their source and mechanism of action remain unclear. Here, we show that by controlling fungi and bacteria captured by splenic macrophages, neutrophil-derived myeloperoxidase attenuates sepsis by suppressing histone release. In systemic candidiasis, microbial capture via the phagocytic receptor SIGNR1 neutralizes myeloperoxidase by facilitating marginal zone infiltra
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Ioannou, M., Hoving, D., Aramburu, I. V., Temkin, M. I., De Vasconcelos, N. M., Tsourouktsoglou, T.-D., Wang, Q., Boeing, S., Goldstone, R., Vernardis, S., Demichev, V., Ralser, M., David, S., Stahl, K., Bode, C., & Papayannopoulos, V. (2022). Microbe capture by splenic macrophages triggers sepsis via T cell-death-dependent neutrophil lifespan shortening. Nature Communications, 13(1), 4658. https://doi.org/10.1038/s41467-022-32320-1
