Innate and adaptive immune responses to fungi in the airway

Fungi are ubiquitous outdoors and indoors. Exposure, sensitization, or both to fungi are strongly associated with development of asthma and allergic airway diseases. Furthermore, global climate change will likely increase the prevalence of fungi and enhance their antigenicity. Major progress has bee...

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Published inJournal of allergy and clinical immunology Vol. 142; no. 2; pp. 353 - 363
Main Authors Bartemes, Kathleen R., Kita, Hirohito
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.08.2018
Elsevier Limited
Subjects
Adaptive Immunity
airway
Allergens - immunology
Allergies
Animals
Antigenicity
Antigens
Antigens, Fungal - immunology
Arthropods
Asthma
Asthma - immunology
Bacteria
Biological activity
CD4 antigen
Cell surface
Chemokines
Chitin
Climate change
Cytokines
Cytokines - metabolism
Dendritic cells
Epithelial cells
Fungi
Fungi - immunology
Gram-positive bacteria
Helper cells
Homeostasis
Human subjects
Humans
Hypersensitivity
Hypersensitivity - immunology
Immune response
Immune system
Immunity, Innate
Inflammation
innate immunity
Lymphocytes
Lymphocytes T
Mycoses - immunology
Neutrophils
Proteins
Respiratory Mucosa - microbiology
Respiratory Mucosa - physiology
Respiratory System - immunology
Respiratory System - microbiology
Respiratory tract diseases
T cell receptors
Th1 Cells - immunology
Th2 Cells - immunology
Viral infections
β-Glucan
ABPM
PAR
TSLP
CRS
MR
airway
Treg
CLR
AHR
RAGE
adaptive immunity
Fungi
ILC2
PRR
innate immunity
DC-SIGN
SPT
AFRS
TLR
SAFS
DC
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Abstract Fungi are ubiquitous outdoors and indoors. Exposure, sensitization, or both to fungi are strongly associated with development of asthma and allergic airway diseases. Furthermore, global climate change will likely increase the prevalence of fungi and enhance their antigenicity. Major progress has been made during the past several years regarding our understanding of antifungal immunity. Fungi contain cell-wall molecules, such as β-glucan and chitin, and secrete biologically active proteases and glycosidases. Airway epithelial cells and innate immune cells, such as dendritic cells, are equipped with cell-surface molecules that react to these fungal products, resulting in production of cytokines and proinflammatory mediators. As a result, the adaptive arm of antifungal immunity, including TH1-, TH2-, and TH17-type CD4+ T cells, is established, reinforcing protection against fungal infection and causing detrimental immunopathology in certain subjects. We are only in the beginning stages of understanding the complex biology of fungi and detailed mechanisms of how they activate the immune response that can protect against or drive diseases in human subjects. Here we describe our current understanding with an emphasis on airway allergic immune responses. The gaps in our knowledge and desirable future directions are also discussed.
AbstractList Fungi are ubiquitous outdoors and indoors. Exposure, sensitization, or both to fungi are strongly associated with development of asthma and allergic airway diseases. Furthermore, global climate change will likely increase the prevalence of fungi and enhance their antigenicity. Major progress has been made during the past several years regarding our understanding of antifungal immunity. Fungi contain cell-wall molecules, such as β-glucan and chitin, and secrete biologically active proteases and glycosidases. Airway epithelial cells and innate immune cells, such as dendritic cells, are equipped with cell-surface molecules that react to these fungal products, resulting in production of cytokines and proinflammatory mediators. As a result, the adaptive arm of antifungal immunity, including TH1-, TH2-, and TH17-type CD4+ T cells, is established, reinforcing protection against fungal infection and causing detrimental immunopathology in certain subjects. We are only in the beginning stages of understanding the complex biology of fungi and detailed mechanisms of how they activate the immune response that can protect against or drive diseases in human subjects. Here we describe our current understanding with an emphasis on airway allergic immune responses. The gaps in our knowledge and desirable future directions are also discussed.
Fungi are ubiquitous outdoors and indoors. Exposure, sensitization, or both to fungi are strongly associated with development of asthma and allergic airway diseases. Furthermore, global climate change will likely increase the prevalence of fungi and enhance their antigenicity. Major progress has been made during the past several years regarding our understanding of antifungal immunity. Fungi contain cell-wall molecules, such as β-glucan and chitin, and secrete biologically active proteases and glycosidases. Airway epithelial cells and innate immune cells, such as dendritic cells, are equipped with cell-surface molecules that react to these fungal products, resulting in production of cytokines and proinflammatory mediators. As a result, the adaptive arm of antifungal immunity, including T 1-, T 2-, and T 17-type CD4 T cells, is established, reinforcing protection against fungal infection and causing detrimental immunopathology in certain subjects. We are only in the beginning stages of understanding the complex biology of fungi and detailed mechanisms of how they activate the immune response that can protect against or drive diseases in human subjects. Here we describe our current understanding with an emphasis on airway allergic immune responses. The gaps in our knowledge and desirable future directions are also discussed.
Fungi are ubiquitous outdoors and indoors. Exposure, sensitization, or both to fungi are strongly associated with development of asthma and allergic airway diseases. Furthermore, global climate change will likely increase the prevalence of fungi and enhance their antigenicity. Major progress has been made during the past several years regarding our understanding of antifungal immunity. Fungi contain cell-wall molecules, such as β-glucan and chitin, and secrete biologically active proteases and glycosidases. Airway epithelial cells and innate immune cells, such as dendritic cells, are equipped with cell-surface molecules that react to these fungal products, resulting in production of cytokines and proinflammatory mediators. As a result, the adaptive arm of antifungal immunity, including TH1-, TH2-, and TH17-type CD4+ T cells, is established, reinforcing protection against fungal infection and causing detrimental immunopathology in certain subjects. We are only in the beginning stages of understanding the complex biology of fungi and detailed mechanisms of how they activate the immune response that can protect against or drive diseases in human subjects. Here we describe our current understanding with an emphasis on airway allergic immune responses. The gaps in our knowledge and desirable future directions are also discussed.Fungi are ubiquitous outdoors and indoors. Exposure, sensitization, or both to fungi are strongly associated with development of asthma and allergic airway diseases. Furthermore, global climate change will likely increase the prevalence of fungi and enhance their antigenicity. Major progress has been made during the past several years regarding our understanding of antifungal immunity. Fungi contain cell-wall molecules, such as β-glucan and chitin, and secrete biologically active proteases and glycosidases. Airway epithelial cells and innate immune cells, such as dendritic cells, are equipped with cell-surface molecules that react to these fungal products, resulting in production of cytokines and proinflammatory mediators. As a result, the adaptive arm of antifungal immunity, including TH1-, TH2-, and TH17-type CD4+ T cells, is established, reinforcing protection against fungal infection and causing detrimental immunopathology in certain subjects. We are only in the beginning stages of understanding the complex biology of fungi and detailed mechanisms of how they activate the immune response that can protect against or drive diseases in human subjects. Here we describe our current understanding with an emphasis on airway allergic immune responses. The gaps in our knowledge and desirable future directions are also discussed.
Fungi are ubiquitous outdoors and indoors. Exposure and/or sensitization to fungi is strongly associated with development of asthma and allergic airway diseases. Furthermore, global climate change will likely increase the prevalence of fungi and enhance their antigenicity. Major progress has been made during the past several years regarding our understanding of antifungal immunity. Fungi contain cell wall molecules, such as β-glucan and chitin, and secrete biologically active proteases and glycosidases. Airway epithelial cells and innate immune cells, such as dendritic cells, are equipped with cell surface molecules that react to these fungal products, resulting in production of cytokines and pro-inflammatory mediators. As a result, the adaptive arm of antifungal immunity, including Th1-, Th2-, and Th17-type CD4 + T cells, is established, reinforcing protection against fungal infection and, by the same token, causing detrimental immunopathology in certain individuals. We are only in the beginning stages of understanding the complex biology of fungi and detailed mechanisms of how they activate the immune response that may protect or drive diseases in humans. Here we describe our current understanding with an emphasis on airway allergic immune responses. The gaps in our knowledge and desirable future directions are also discussed.
Author Bartemes, Kathleen R.
Kita, Hirohito
AuthorAffiliation 2 Department of Immunology, Mayo Clinic, Rochester, MN 55905
1 Division of Allergic Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905
AuthorAffiliation_xml – name: 2 Department of Immunology, Mayo Clinic, Rochester, MN 55905
– name: 1 Division of Allergic Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905
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  givenname: Hirohito
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  fullname: Kita, Hirohito
  email: kita.hirohito@mayo.edu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30080527$$D View this record in MEDLINE/PubMed
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Copyright 2018 American Academy of Allergy, Asthma & Immunology
Copyright © 2018 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
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Sun Apr 06 06:53:19 EDT 2025
Tue Aug 26 16:36:28 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 2
Keywords ABPM
PAR
TSLP
CRS
MR
airway
Treg
CLR
AHR
RAGE
adaptive immunity
Fungi
ILC2
PRR
innate immunity
DC-SIGN
SPT
AFRS
TLR
SAFS
DC
Language English
License Copyright © 2018 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
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Snippet Fungi are ubiquitous outdoors and indoors. Exposure, sensitization, or both to fungi are strongly associated with development of asthma and allergic airway...
Fungi are ubiquitous outdoors and indoors. Exposure and/or sensitization to fungi is strongly associated with development of asthma and allergic airway...
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SubjectTerms Adaptive Immunity
airway
Allergens - immunology
Allergies
Animals
Antigenicity
Antigens
Antigens, Fungal - immunology
Arthropods
Asthma
Asthma - immunology
Bacteria
Biological activity
CD4 antigen
Cell surface
Chemokines
Chitin
Climate change
Cytokines
Cytokines - metabolism
Dendritic cells
Epithelial cells
Fungi
Fungi - immunology
Gram-positive bacteria
Helper cells
Homeostasis
Human subjects
Humans
Hypersensitivity
Hypersensitivity - immunology
Immune response
Immune system
Immunity, Innate
Inflammation
innate immunity
Lymphocytes
Lymphocytes T
Mycoses - immunology
Neutrophils
Proteins
Respiratory Mucosa - microbiology
Respiratory Mucosa - physiology
Respiratory System - immunology
Respiratory System - microbiology
Respiratory tract diseases
T cell receptors
Th1 Cells - immunology
Th2 Cells - immunology
Viral infections
β-Glucan
Title Innate and adaptive immune responses to fungi in the airway
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0091674918309242
https://dx.doi.org/10.1016/j.jaci.2018.06.015
https://www.ncbi.nlm.nih.gov/pubmed/30080527
https://www.proquest.com/docview/2082046680
https://www.proquest.com/docview/2084919868
https://pubmed.ncbi.nlm.nih.gov/PMC6083885
Volume 142
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