Airway epithelial cells condition dendritic cells to express multiple immune surveillance genes

Rate, Angela, Bosco, Anthony, McKenna, Kathy L., Holt, Patrick G. and Upham, John W. (2012) Airway epithelial cells condition dendritic cells to express multiple immune surveillance genes. PLoS One, 7 9 Article No. e44941: . doi:10.1371/journal.pone.0044941


Author Rate, Angela
Bosco, Anthony
McKenna, Kathy L.
Holt, Patrick G.
Upham, John W.
Title Airway epithelial cells condition dendritic cells to express multiple immune surveillance genes
Journal name PLoS One   Check publisher's open access policy
ISSN 1932-6203
Publication date 2012-09
Sub-type Article (original research)
DOI 10.1371/journal.pone.0044941
Volume 7
Issue 9 Article No. e44941
Total pages 10
Place of publication San Francisco, CA United States
Publisher Public Library of Science
Collection year 2013
Language eng
Formatted abstract Increasing evidence suggests that crosstalk between airway epithelial cells (AEC) and adjacent dendritic cells (DC) tightly regulates airway mucosal DC function in steady state. AEC are known to express multiple immmuno-modulatory factors, though detailed information on how this influences human DC function remains incomplete. We recently demonstrated using an in vitro coculture model that AEC alter differentiation of monocytes into DC in a manner that inhibits expression of potentially damaging Th2 effector function. In the current study, we have extended these findings to examine other aspects of DC function. Using micro-array technology we show that multiple genes important for immune surveillance are significantly over expressed in purified AEC-conditioned DC, compared to control DC. These findings were confirmed by quantitative real time PCR or flow cytometry in an independent sample set. In particular, AEC-conditioned DC showed selective upregulation of chemokines that recruit Th1 cells, but minimal change in chemokines linked to Th2 cell recruitment. AEC-conditioned DC were also characterized by enhanced expression of complement family genes (C1QB, C2, CD59 and SERPING1), Fcγ receptor genes (FCGR1A, FCGR2A, FCGR2B and FCGR2C), signaling lymphocytic activation molecule family member 1 (SLAM), programmed death ligands 1 and 2, CD54 and CD200R1, relative to control DC. These findings suggest that AEC conditioning facilitates the capacity of DC to react to danger signals, to enhance leukocyte recruitment, especially of Th1 effector cells, and to interact with other immune cell populations while minimizing the risks of excessive inflammation leading to tissue damage
Keyword Lung Inflammation
Differential Expression
Chemokine Receptors
Cross Presentation
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2013 Collection
School of Medicine Publications
 
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