PMID- 23352530
OWN - NLM
STAT- MEDLINE
DCOM- 20130402
LR  - 20130128
IS  - 1534-4436 (Electronic)
IS  - 1081-1206 (Linking)
VI  - 110
IP  - 2
DP  - 2013 Feb
TI  - Effect of mite allergen immunotherapy on the altered phenotype of dendritic cells 
      in allergic asthmatic children.
PG  - 107-12
LID - S1081-1206(12)00945-3 [pii]
LID - 10.1016/j.anai.2012.11.019 [doi]
AB  - BACKGROUND: Allergic asthma is a T(H)2 inflammatory disease. Dendritic cells 
      (DCs) play key roles in the T(H)1/T(H)2 balance. Allergen specific immunotherapy 
      (SIT) has the potential to modify the course of allergy because the ratio of 
      T(H)1 to T(H)2 cytokines produced is increased after SIT. OBJECTIVE: To determine 
      how SIT affects DCs in children and to define novel parameters of this treatment. 
      METHODS: We investigated the changes of phenotypic and functional variations of 
      monocyte-derived DCs from allergic asthmatic children undergoing complete mite 
      SIT. Peripheral blood monocytes from SIT allergic asthmatic children, allergic 
      asthmatic controls, and healthy controls were cultured with 
      granulocyte-macrophage colony-stimulating factor and interleukin 4 and then 
      stimulated with Dermatophagoides pteronyssinus (Der p) allergen or 
      lipopolysaccharide (LPS). The expressions of surface molecules on 
      monocyte-derived DCs were assessed by flow cytometry. Cytokine production by 
      cultured monocyte-derived DCs was determined by enzyme-linked immunosorbent 
      assay. RESULTS: After LPS stimulation, monocyte-derived DCs of the allergic 
      asthmatic group had a higher CD86 and lower HLA-DR expression than the healthy 
      controls. In SIT patients, the expression was similar to that of the healthy 
      controls. After Der p stimulation monocyte-derived DCs of the allergic asthmatic 
      patients displayed lower Toll-like receptor 4 (TLR4), whereas again in SIT 
      patients the expression was similar to that of healthy controls. CONCLUSION: 
      These findings indicate that SIT normalizes the expression of CD86, HLA-DR, and 
      TLR4 on DCs. Moreover, CD86, HLA-DR, and TLR4 may be useful parameters for 
      monitoring SIT. Decreased TLR4 expression in allergic asthmatic patients might be 
      compensated by TLR4 agonists, with the potential of amplifying the effects of 
      SIT.
CI  - Copyright (c) 2013 American College of Allergy, Asthma & Immunology. Published by 
      Elsevier Inc. All rights reserved.
FAU - Wang, Chuang-Ming
AU  - Wang CM
AD  - Department of Pediatrics, Ditmanson Medical Foundation Chia-Yi Christian 
      Hospital, Chiayi, Taiwan.
FAU - Chuang, Jing-Jing
AU  - Chuang JJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121221
PL  - United States
TA  - Ann Allergy Asthma Immunol
JT  - Annals of allergy, asthma & immunology : official publication of the American 
      College of Allergy, Asthma, & Immunology
JID - 9503580
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 4)
RN  - 130068-27-8 (Interleukin-10)
RN  - 187348-17-0 (Interleukin-12)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Adolescent
MH  - Animals
MH  - Asthma/immunology/*therapy
MH  - Child
MH  - Dendritic Cells/*immunology
MH  - *Desensitization, Immunologic
MH  - Female
MH  - HLA-DR Antigens/analysis
MH  - Humans
MH  - Immunoglobulin E/blood
MH  - Interleukin-10/biosynthesis
MH  - Interleukin-12/biosynthesis
MH  - Lipopolysaccharides/pharmacology
MH  - Male
MH  - Mites/*immunology
MH  - Phenotype
MH  - Toll-Like Receptor 4/physiology
EDAT- 2013/01/29 06:00
MHDA- 2013/04/03 06:00
CRDT- 2013/01/29 06:00
PHST- 2012/08/08 00:00 [received]
PHST- 2012/11/22 00:00 [revised]
PHST- 2012/11/26 00:00 [accepted]
PHST- 2013/01/29 06:00 [entrez]
PHST- 2013/01/29 06:00 [pubmed]
PHST- 2013/04/03 06:00 [medline]
AID - S1081-1206(12)00945-3 [pii]
AID - 10.1016/j.anai.2012.11.019 [doi]
PST - ppublish
SO  - Ann Allergy Asthma Immunol. 2013 Feb;110(2):107-12. doi: 
      10.1016/j.anai.2012.11.019. Epub 2012 Dec 21.