PMID- 17823633
OWN - NLM
STAT- MEDLINE
DCOM- 20071214
LR  - 20070907
IS  - 0008-4212 (Print)
IS  - 0008-4212 (Linking)
VI  - 85
IP  - 7
DP  - 2007 Jul
TI  - Dendritic cells in allergic airway inflammation.
PG  - 686-99
AB  - Dendritic cells (DCs) are primary antigen-presenting cells involved in 
      interactions with T cells leading to the proliferation of TH1 or TH2 cell types. 
      In asthma, predominance of TH2 cells appears to be responsible for disease 
      pathogenesis. Differentiation of TH2 cells is driven by a variety of factors such 
      as the expression of high levels of costimulatory molecules, the cytokine 
      profile, and the subset of DCs. Many inflammatory cells involved in the 
      pathogenesis of asthma either directly or indirectly modulate DC function. 
      Traditional treatments for asthma decrease the number of airway DCs in animals as 
      well as in patients with asthma. Immunomodulators including interleukin (IL)-10, 
      transforming growth factor (TGF)-beta, cytosine-phosphate-guanosine-containing 
      oligodeoxynucleotides (CpG-ODN), 1alpha,25-dihydroxyvitamin D3, and fetal liver 
      tyrosine kinase 3 ligand (Flt3L) are involved in the modulation of the function 
      of DCs. Based on the critical review of the interaction between DCs and other 
      inflammatory cells, we propose that activation of T cells by DCs and 
      sensitization to inhaled allergen and resulting airway inflammation are dependent 
      on plasmacytoid and myeloid subset of lung DCs to induce an immune response or 
      tolerance and are tightly regulated by T-regulatory cells. Effects of various 
      therapeutic agents to modulate the function of lung myeloid DCs have been 
      discussed.
FAU - Bharadwaj, Arpita S
AU  - Bharadwaj AS
AD  - Department of Medical Microbiology, Creighton University School of Medicine, 
      CRISS II, Room 510, California Plaza, Omaha, NE 68178, USA.
FAU - Bewtra, Againdra K
AU  - Bewtra AK
FAU - Agrawal, Devendra K
AU  - Agrawal DK
LA  - eng
GR  - R01 HL070885/HL/NHLBI NIH HHS/United States
GR  - R01 HL073349/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - Canada
TA  - Can J Physiol Pharmacol
JT  - Canadian journal of physiology and pharmacology
JID - 0372712
RN  - 0 (Anti-Asthmatic Agents)
SB  - IM
MH  - Animals
MH  - Anti-Asthmatic Agents/pharmacology/therapeutic use
MH  - Antigen Presentation/immunology
MH  - Asthma/drug therapy/*immunology
MH  - Cell Communication/immunology
MH  - Dendritic Cells/drug effects/*immunology/metabolism
MH  - Humans
MH  - Models, Immunological
MH  - Respiratory Hypersensitivity/drug therapy/*immunology
MH  - T-Lymphocytes/immunology
RF  - 156
EDAT- 2007/09/08 09:00
MHDA- 2007/12/15 09:00
CRDT- 2007/09/08 09:00
PHST- 2007/09/08 09:00 [pubmed]
PHST- 2007/12/15 09:00 [medline]
PHST- 2007/09/08 09:00 [entrez]
AID - y07-062 [pii]
AID - 10.1139/Y07-062 [doi]
PST - ppublish
SO  - Can J Physiol Pharmacol. 2007 Jul;85(7):686-99. doi: 10.1139/Y07-062.