title: Current understanding of allergic fungal rhinosinusitis and treatment implications.
abstract: OBJECTIVE
  The pathophysiology of allergic fungal rhinosinusitis (AFRS) is not fully understood and is in constant evolution. Although initial theories favored an immunoglobulin E-mediated immune response to fungal antigens as having a primary role in the immunopathologic process of AFRS, the purpose of this review is to highlight recent studies that suggest a more complex, epithelial cell-driven immune response being central to the pathophysiology of the disease. Treatment implications are considered.
  
  
  RESULTS
  Recent studies demonstrate a central role of cytokines derived from respiratory epithelial cells, including interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin, in the orchestration of both innate and adaptive T helper 2 immune responses that are important components of the immunopathology of chronic rhinosinusitis with nasal polyposis and AFRS. In addition, the robust Th2 adaptive response may be mediated by both fungal antigens and Staphylococcus aureus superantigens.
  
  
  CONCLUSIONS
  Given the evolving understanding of AFRS pathophysiology, management continues to maintain a broad focus on minimizing the burden of the inflammatory trigger(s) and suppressing the inflammatory cascade. This is primarily accomplished through surgery and corticosteroid therapy. Immunotherapy, antimicrobial therapy, and other immunomodulatory medications may help mediate the disease process as well.
authors.affiliation: Department of Otorhinolaryngology, Head and Neck Surgery, University of Texas Medical School at Houston, Houston, Texas, USA.
authors.forename: Drew P
authors.initials: DP
authors.lastname: Plonk
authors.forename: Amber
authors.initials: A
authors.lastname: Luong
mesh_terms: D006801:Humans; D009181:Mycoses / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy*; D065631:Rhinitis, Allergic / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy*; D012852:Sinusitis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy*