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. 2021 Nov 18;12:785883. doi: 10.3389/fimmu.2021.785883

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Copyright © 2021 Parente, Possetti, Erreni, D’Autilia, Bottazzi, Garlanda, Mantovani, Inforzato and Doni

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Complement-dependent roles of PTX3 and SAP in the host resistance to A. fumigatus. (A) PTX3 and Ficolin-2 recruit each other onto AF conidia, and activate the LP. As C3b and iC3b deposit (via the AP amplification loop), PTX3 promotes phagocytosis of AF via FcγRII (CD32)-dependent redistribution of CD11b (that forms with CD18 the complement receptor 3, CR3, major receptor of iC3b) to the phagocytic cup. (B) SAP recruits C1q to AF conidia, and promotes CP activation. This leads to enhanced disposal of the pathogen through neutrophil-dependent phagocytosis and MAC-mediated killing.