Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 109, Issue 6, Pages S521-S524Publisher
MOSBY, INC
DOI: 10.1067/mai.2002.124564
Keywords
atopy; environment; pediatric asthma; genetics; pathogenesis
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Funding
- NHLBI NIH HHS [HL-56396, HL-61979] Funding Source: Medline
- NIAID NIH HHS [AI-34691] Funding Source: Medline
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Asthma is a heterogeneous disease characterized by varying phenotypes. Ongoing research is focused on identifying which children who have wheezing early will progress to childhood asthma. Genetic factors, predominantly atopy and a parental history of asthma as well as environmental stimuli, are key components in the development of asthma. Investigation into immunologic processes indicates that atopic children may have a cytokine imbalance or dysregulation in which the transition from T helper 2 (T(H)2)-type to T(H)1-type immunity is delayed. Several risk factors have been identified in the pathophysiology of asthma, including sensitization and exposure to cockroaches, house dust mites, and the mold Allernaria alternata, among other aeroallergens. Viral respiratory infections, primarily those caused by respiratory syncytial virus, are a significant risk factor for the development of childhood wheezing in the first decade of life. A number of prospective epidemiologic studies are investigating, among other issues, the relations among cytokine dysregulation, respiratory tract infections, and allergen exposure and sensitization in the development of asthma. Identifying the pathogenic mechanisms should enable clinicians to identify children at high risk and thereby to treat childhood asthma more effectively.
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