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Innate immunity in the lung regulates the development of asthma.
- Source :
-
Immunological reviews [Immunol Rev] 2014 Jul; Vol. 260 (1), pp. 235-48. - Publication Year :
- 2014
-
Abstract
- The lung, while functioning as a gas exchange organ, encounters a large array of environmental factors, including particulate matter, toxins, reactive oxygen species, chemicals, allergens, and infectious microbes. To rapidly respond to and counteract these elements, a number of innate immune mechanisms have evolved that can lead to lung inflammation and asthma, which is the focus of this review. These innate mechanisms include a role for two incompletely understood cell types, invariant natural killer T (iNKT) cells and innate lymphoid cells (ILCs), which together produce a wide range of cytokines, including interleukin-4 (IL-4), IL-5, IL-13, interferon-γ, IL-17, and IL-22, independently of adaptive immunity and conventional antigens. The specific roles of iNKT cells and ILCs in immunity are still being defined, but both cell types appear to play important roles in the lungs, particularly in asthma. As we gain a better understanding of these innate cell types, we will acquire great insight into the mechanisms by which allergic and non-allergic asthma phenotypes develop.<br /> (© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
- Subjects :
- Adaptive Immunity
Allergens immunology
Animals
Asthma genetics
Asthma metabolism
Asthma microbiology
Cell Communication
Humans
Lung metabolism
Lung microbiology
Lymphocytes immunology
Lymphocytes metabolism
Natural Killer T-Cells immunology
Natural Killer T-Cells metabolism
Respiratory Hypersensitivity genetics
Respiratory Hypersensitivity immunology
Respiratory Hypersensitivity metabolism
Respiratory Hypersensitivity microbiology
Asthma immunology
Immunity, Innate
Lung immunology
Subjects
Details
- Language :
- English
- ISSN :
- 1600-065X
- Volume :
- 260
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Immunological reviews
- Publication Type :
- Academic Journal
- Accession number :
- 24942693
- Full Text :
- https://doi.org/10.1111/imr.12187