Document Detail


Immune dysregulation in the pathogenesis of pulmonary alveolar proteinosis.
MedLine Citation:
PMID:  20623372     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pulmonary alveolar proteinosis (PAP) is a rare disease of the lung characterized by the accumulation of surfactant-derived lipoproteins within pulmonary alveolar macrophages and alveoli, resulting in respiratory insufficiency and increased infections. The disease is caused by a disruption in surfactant catabolism by alveolar macrophages due to loss of functional granulocyte-macrophage colony-stimulating factor (GM-CSF) signaling. The underlying molecular mechanisms causing deficiencies in GM-CSF signaling are as follows: 1) high levels of neutralizing GM-CSF autoantibodies observed in autoimmune PAP; 2) mutations in CSF2RA, the gene encoding the alpha chain of the GM-CSF receptor, observed in hereditary PAP; and 3) reduced numbers and function of alveolar macrophages as a result of other clinical diseases seen in secondary PAP. Recent studies investigating the biology of GM-CSF have revealed that not only does this cytokine have an indispensable role in lung physiology, but it is also a critical regulator of innate immunity and lung host defense.
Authors:
Margarita Martinez-Moczygemba; David P Huston
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Current allergy and asthma reports     Volume:  10     ISSN:  1534-6315     ISO Abbreviation:  Curr Allergy Asthma Rep     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-07-23     Completed Date:  2010-12-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101096440     Medline TA:  Curr Allergy Asthma Rep     Country:  United States    
Other Details:
Languages:  eng     Pagination:  320-5     Citation Subset:  IM    
Affiliation:
Departments of Microbial and Molecular Pathogenesis and Medicine, College of Medicine and Clinical Science and Translational Research Institute, Texas A&M Health Science Center, 2121 West Holcombe Boulevard, Houston, TX 77030, USA. mmoczygemba@medicine.tamhsc.edu
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MeSH Terms
Descriptor/Qualifier:
Antibodies, Neutralizing / immunology
Antibody Specificity
Autoimmunity / immunology
Cell Count
Humans
Lipoproteins / metabolism
Macrophages, Alveolar / immunology,  pathology
Mutation
Pulmonary Alveolar Proteinosis / immunology*,  physiopathology*,  therapy
Pulmonary Alveoli / physiopathology
Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / genetics,  immunology*,  metabolism
Signal Transduction
Grant Support
ID/Acronym/Agency:
AI063178/AI/NIAID NIH HHS; AI36936/AI/NIAID NIH HHS; U19AI071130/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies, Neutralizing; 0/CSF2RA protein, human; 0/Lipoproteins; 0/Receptors, Granulocyte-Macrophage Colony-Stimulating Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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