27 March 2024 | Jata Shankar, Raman Thakur, Karl V. Clemons, David A. Stevens
Aspergillosis, a fungal infection caused by various species of *Aspergillus*, particularly *A. fumigatus*, can manifest as allergic bronchopulmonary aspergillosis, aspergilloma, chronic pulmonary aspergillosis, and invasive aspergillosis. The clinical severity and manifestations vary based on individual immune status and the specific species of *Aspergillus*. Pathogen-associated molecular patterns (PAMPs) such as glucan, galactomannan, mannose, and conidial surface proteins are recognized by pathogen recognition receptors (PRRs) on immune cells, including Toll-like receptors (TLRs) and C-type lectins (Dectin-1 and Dectin-2). Cytokines and chemokines play crucial roles in the immune response to *Aspergillus* infection, with IFN-γ, TNF-α, CCR4, CCR17, and various interleukins (ILs) being key players. For instance, allergic bronchopulmonary aspergillosis (ABPA) is characterized by Th2 and Th9 cell-type immunity, involving IL-4, IL-5, IL-13, and IL-10, while invasive aspergillosis involves Th1 and Th17 cell-type immunity via IFN-γ, IL-1, IL-6, and IL-17. These cytokines activate immune cells, stimulate the production of antimicrobial peptides and reactive oxygen species, and help in the clearance of the fungal pathogen. Understanding the interplay between host responses and *Aspergillus* infection, both in humans and animals, can aid in developing precise immunotherapeutic strategies, potentially advancing personalized medicine.Aspergillosis, a fungal infection caused by various species of *Aspergillus*, particularly *A. fumigatus*, can manifest as allergic bronchopulmonary aspergillosis, aspergilloma, chronic pulmonary aspergillosis, and invasive aspergillosis. The clinical severity and manifestations vary based on individual immune status and the specific species of *Aspergillus*. Pathogen-associated molecular patterns (PAMPs) such as glucan, galactomannan, mannose, and conidial surface proteins are recognized by pathogen recognition receptors (PRRs) on immune cells, including Toll-like receptors (TLRs) and C-type lectins (Dectin-1 and Dectin-2). Cytokines and chemokines play crucial roles in the immune response to *Aspergillus* infection, with IFN-γ, TNF-α, CCR4, CCR17, and various interleukins (ILs) being key players. For instance, allergic bronchopulmonary aspergillosis (ABPA) is characterized by Th2 and Th9 cell-type immunity, involving IL-4, IL-5, IL-13, and IL-10, while invasive aspergillosis involves Th1 and Th17 cell-type immunity via IFN-γ, IL-1, IL-6, and IL-17. These cytokines activate immune cells, stimulate the production of antimicrobial peptides and reactive oxygen species, and help in the clearance of the fungal pathogen. Understanding the interplay between host responses and *Aspergillus* infection, both in humans and animals, can aid in developing precise immunotherapeutic strategies, potentially advancing personalized medicine.