PMID- 18640476
OWN - NLM
STAT- MEDLINE
DCOM- 20081022
LR  - 20130118
IS  - 0149-2918 (Print)
IS  - 0149-2918 (Linking)
VI  - 30 Spec No
DP  - 2008
TI  - Respiratory virus and asthma: the role of immunoglobulin E.
PG  - 1017-24
LID - 10.1016/j.clinthera.2008.06.002 [doi]
AB  - BACKGROUND: Atopic diseases, including asthma, have increased to epidemic 
      proportions in the westernized world. The reasons for this increase are not 
      known, nor are the mechanisms behind the development of these diseases. An 
      interesting aspect of atopic disease is the role of respiratory viruses in the 
      development of asthma and atopy. In fact, severe respiratory viral infection in 
      infancy has been associated with a greatly increased risk of asthma. OBJECTIVE: 
      This paper explores potential mechanisms through which viruses impart an 
      increased risk of asthma, focusing on new pathways in mouse models of atopy. 
      METHODS: A search of MEDLINE (1950-March 2008) was conducted using terms that 
      included viral-induced wheeze, respiratory virus, asthma, IgE, and dendritic 
      cells. RESULTS: A total of 1643 publications were identified that contained > or 
      = 1 of the search terms; however, only 7 of these focused on immunoglobulin E 
      (IgE) and the viral risk of asthma, and only 1 of the 7 explored the role of 
      dendritic cells in this process. The latter study suggested a mechanistic link 
      between lung dendritic cells and the development of postviral atopic disease. 
      Important in this pathway is the generation of IgE, its high-affinity receptor, 
      and the T-cell chemoattractant CCL28. CONCLUSIONS: Data from recent mouse models 
      suggest that the development of asthma after severe respiratory viral infection 
      may be the result of a response generated by production of antiviral IgE, which 
      is capable of engaging dendritic cells to form a chemoattractant for 
      interleukin-13-producing T cells. This new paradigm points to a focus for 
      development of future therapies to prevent or at least ameliorate post- viral 
      atopic disease.
FAU - Khan, Sadia Hayat
AU  - Khan SH
AD  - Division of Allergy and Immunology, Department of Internal Medicine, Washington 
      University School of Medicine, Saint Louis, Missouri, USA.
FAU - Park, Stephanie S
AU  - Park SS
FAU - Sirajuddin, Iram A
AU  - Sirajuddin IA
FAU - Grayson, Mitchell H
AU  - Grayson MH
LA  - eng
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Clin Ther
JT  - Clinical therapeutics
JID - 7706726
RN  - 0 (Antibodies, Anti-Idiotypic)
RN  - 0 (anti-IgE antibodies)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Animals
MH  - Antibodies, Anti-Idiotypic/immunology
MH  - Asthma/etiology/*immunology/therapy
MH  - Dendritic Cells/immunology
MH  - Humans
MH  - Immunoglobulin E/*immunology
MH  - Lung/immunology
MH  - Respiratory Syncytial Virus Infections/*complications/immunology
MH  - Respiratory Tract Infections/*complications/immunology/virology
EDAT- 2008/07/22 09:00
MHDA- 2008/10/23 09:00
CRDT- 2008/07/22 09:00
PHST- 2008/04/25 00:00 [received]
PHST- 2008/07/22 09:00 [pubmed]
PHST- 2008/10/23 09:00 [medline]
PHST- 2008/07/22 09:00 [entrez]
AID - S0149-2918(08)00203-8 [pii]
AID - 10.1016/j.clinthera.2008.06.002 [doi]
PST - ppublish
SO  - Clin Ther. 2008;30 Spec No:1017-24. doi: 10.1016/j.clinthera.2008.06.002.