“…Indeed, reduced cell adhesion, phagocytosis, pathogen killing, mannose-and Toll-like receptor expression, and LPS-or peptidoglycan-stimulated TNFα release were observed in alveolar macrophages and neutrophils from GM-CSF deficient mice and PAP patients [31,35]. Accordingly, PAP patients developed respiratory and extrapulmonary infections with opportunistic pathogens such as nontuberculous mycobacteria, Histoplasma, Cryptococcus, Nocardia or fungi [35][36][37][38][39][40]. Notably, this spectrum of infections appears very similar to the phenotype associated with the presence of neutralizing anti-IFNγ AAbs [6].…”