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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Leukoc+Biol
2017 ; 102
(4
): 965-976
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Frontline Science: Shh production and Gli signaling is activated in vivo in lung,
enhancing the Th2 response during a murine model of allergic asthma
#MMPMID28235772
Standing ASI
; Yánez DC
; Ross R
; Crompton T
; Furmanski AL
J Leukoc Biol
2017[Oct]; 102
(4
): 965-976
PMID28235772
show ga
The pathophysiology of allergic asthma is driven by Th2 immune responses after
aeroallergen inhalation. The mechanisms that initiate, potentiate, and regulate
airway allergy are incompletely characterized. We have shown that Hh signaling to
T cells, via downstream Gli transcription factors, enhances T cell conversion to
a Th2 phenotype. In this study, we showed for the first time, to our knowledge,
that Gli-dependent transcription is activated in T cells in vivo during murine
AAD, a model for the immunopathology of asthma, and that genetic repression of
Gli signaling in T cells decreases the differentiation and recruitment of Th2
cells to the lung. T cells were not the only cells that expressed activated Gli
during AAD. A substantial proportion of eosinophils and lung epithelial cells,
both central mediators of the immunopathology of asthma, also underwent Hh/Gli
signaling. Finally, Shh increased Il-4 expression in eosinophils. We therefore
propose that Hh signaling during AAD is complex, involving multiple cell types,
signaling in an auto- or paracrine fashion. Improved understanding of the role of
this major morphogenetic pathway in asthma may give rise to new drug targets for
this chronic condition.