How do airborne fungal spores avoid immune recognition? (40.1)

Abstract

Abstract Every day we inhale thousands of tiny fungal spores (conidia), originating from many different fungal species such as Aspergillus, Cladosporium, Penicillium and Alternaria. Although these spores are packed with antigens and allergens, yet their inhalation does not continuously activate our innate immune cells or provoke inflammatory responses. By using several fungal inhabitants of the air-borne microflora including the human opportunistic fungal pathogen Aspergillus fumigatus, in vitro assays using human dendritic cells (DC) and alveolar macrophages (AM) and in vivo experiments using a murine model we show that a protein surface-layer called ‘rodlet’ on the dormant conidia masks their recognition by the immune system and hence prevents immune response to conidia. Interestingly, rodlet proteins are found to be immunologically inert and failed to activate either human or mouse DC and AM and did not induce adaptive T responses in vivo upon transfer of rodlet-pulsed DC. Furthermore, dormant conidia that lacked rodlet layer induced strong immune responses in vitro and in vivo despite being dormant in nature. All these results indicate that rodlet layer on dormant conidia masks the immunogenic molecules and prevent immune aggression against inhaled conidia.