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A new RelB‐dependent CD117 + CD172a + murine DC subset preferentially induces Th2 differentiation and supports airway hyperresponses in vivo

Authors :
Tim Sparwasser
Carla N. Castro
Christian Engelmann
Nico Andreas
Thomas Kamradt
Marco Groth
Ronny Haenold
Marc Riemann
Ievgen O. Koliesnik
Falk Weih
Source :
European Journal of Immunology. 48:923-936
Publication Year :
2018
Publisher :
Wiley, 2018.

Abstract

The NF-κB transcription factor subunit RelB is important for the full activation of conventional dendritic cells (cDCs) during T-cell-dependent immune responses. Although the number of splenic DCs is greatly reduced in RelBnull mice, the cause and consequences of this deficiency are currently unknown. To circumvent the impact of the pleiotropic defects in RelBnull mice we used a reporter model for RelB expression (RelBKatushka mice) and conditionally deleted RelB in DCs (RelBCD11c-Cre mice). Thereby, we can show here that RelB is essential for the differentiation of a CD117+ CD172a+ cDC subpopulation that highly expresses RelB. Surprisingly, these DCs depend on p50 for their development and are negatively regulated by a constitutive p52 activation in absence of p100. The absence of p52/p100 had no influence on the homeostasis of CD117+ CD172a+ cDCs. RelB-dependent CD117+ CD172a+ DCs strongly induce the production of the type 2 cytokines IL-4 and IL-13, as well as GM-CSF from naive Th cells. Consequently, mice lacking RelB in cDCs show an attenuated bronchial hyperresponsiveness with reduced eosinophil infiltration. Taken together, we have identified a new splenic RelB-dependent CD117+ CD172a+ cDC population that preferentially induces Th2 responses.

Details

ISSN :
15214141 and 00142980
Volume :
48
Database :
OpenAIRE
Journal :
European Journal of Immunology
Accession number :
edsair.doi...........86330029632f2b3a18d92ad0db2a9d6a
Full Text :
https://doi.org/10.1002/eji.201747332