PMID- 21624504
OWN - NLM
STAT- MEDLINE
DCOM- 20120213
LR  - 20211020
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Print)
IS  - 1567-5769 (Linking)
VI  - 11
IP  - 10
DP  - 2011 Oct
TI  - The active contribution of Toll-like receptors to allergic airway inflammation.
PG  - 1391-8
LID - 10.1016/j.intimp.2011.05.003 [doi]
AB  - Epithelia lining the respiratory tract represent a major portal of entry for 
      microorganisms and allergens and are equipped with innate and adaptive immune 
      signaling receptors for host protection. These include Toll-like receptors (TLRs) 
      that recognize microbial components and evoke diverse responses in cells of the 
      respiratory system. TLR stimulation by microorganism-derived molecules activates 
      antigen presenting cells, control T helper (Th) 1, Th2, and Th17 immune cell 
      differentiation, cytokine production by mast cells, and activation of 
      eosinophils. It is clear that TLR are involved in the pathophysiology of allergic 
      airway diseases such as asthma. Dendritic cells (DCs), a kind of antigen 
      presenting cells, which play a key role in the induction of allergic airway 
      inflammation, are privileged targets for pathogen associated molecular patterns 
      (PAMPs). During the allergic responses, engagement of TLRs on DCs determines the 
      Th2 polarization of the T cells. TLR signaling in mast cells increases the 
      release of IL-5, and TLR activation of airway epithelial cells forces the 
      generation of proallergic Th2 type of cytokines. Although these responses aim to 
      protect the host, they may also result in inflammatory tissue damage in the 
      airway. Under certain conditions, stimulation of TLRs, in particular, TLR9, may 
      reduce Th2-dependent allergic inflammation by induction of Th1 responses. 
      Therefore, understanding the complex regulatory roles of TLRs in the pathogenesis 
      of allergic airway inflammation should facilitate the development of preventive 
      and therapeutic measures for asthmatic patients.
CI  - Copyright (c) 2011 Elsevier B.V. All rights reserved.
FAU - Chen, Keqiang
AU  - Chen K
AD  - Laboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center 
      for Cancer Research, National Cancer Institute at Frederick, Frederick, MD 21702, 
      United States.
FAU - Xiang, Yi
AU  - Xiang Y
FAU - Yao, Xiaohong
AU  - Yao X
FAU - Liu, Ying
AU  - Liu Y
FAU - Gong, Wanghua
AU  - Gong W
FAU - Yoshimura, Teizo
AU  - Yoshimura T
FAU - Wang, Ji Ming
AU  - Wang JM
LA  - eng
GR  - HHSN261200800001C/RC/CCR NIH HHS/United States
GR  - HHSN261200800001E/CA/NCI NIH HHS/United States
GR  - Z01 BC010015/Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, N.I.H., Intramural
PT  - Review
DEP - 20110531
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Interleukin-5)
RN  - 0 (Toll-Like Receptors)
SB  - IM
MH  - Animals
MH  - Antigen Presentation
MH  - Asthma/drug therapy/*immunology
MH  - Cell Differentiation
MH  - Dendritic Cells/immunology
MH  - Eosinophils/*immunology
MH  - Humans
MH  - Interleukin-5/immunology
MH  - Mast Cells/*immunology
MH  - Molecular Targeted Therapy
MH  - Respiratory Mucosa/immunology
MH  - Signal Transduction/immunology
MH  - Th1-Th2 Balance
MH  - Th2 Cells/*immunology
MH  - Toll-Like Receptors/*immunology
PMC - PMC7398422
MID - NIHMS1608727
EDAT- 2011/06/01 06:00
MHDA- 2012/02/14 06:00
PMCR- 2020/08/03
CRDT- 2011/06/01 06:00
PHST- 2011/03/10 00:00 [received]
PHST- 2011/05/02 00:00 [accepted]
PHST- 2011/06/01 06:00 [entrez]
PHST- 2011/06/01 06:00 [pubmed]
PHST- 2012/02/14 06:00 [medline]
PHST- 2020/08/03 00:00 [pmc-release]
AID - S1567-5769(11)00214-1 [pii]
AID - 10.1016/j.intimp.2011.05.003 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2011 Oct;11(10):1391-8. doi: 10.1016/j.intimp.2011.05.003. 
      Epub 2011 May 31.