Resident CD11b+Ly6C- Lung Dendritic Cells Are Responsible for Allergic Airway Sensitization to House Dust Mite in Mice

被引:52
作者
Mesnil, Claire [1 ,2 ]
Sabatel, Catherine M. [1 ,2 ]
Marichal, Thomas [1 ,2 ]
Toussaint, Marie [1 ,2 ]
Cataldo, Didier [3 ]
Drion, Pierre-Vincent [4 ]
Lekeux, Pierre [1 ,2 ]
Bureau, Fabrice [1 ,2 ]
Desmet, Christophe J. [1 ,2 ]
机构
[1] Univ Liege, Lab Cellular & Mol Immunol, GIGA Res, Liege, Belgium
[2] Univ Liege, Fac Vet Med, Liege, Belgium
[3] Univ Liege, Lab Tumours & Dev Biol, GIGA Res, Liege, Belgium
[4] Univ Liege, Lab Preclin & Biomed Sci, Univ Hosp Ctr, Liege, Belgium
来源
PLOS ONE | 2012年 / 7卷 / 12期
关键词
TH2; RESPONSES; T-CELLS; GM-CSF; IMMUNE-RESPONSES; IN-VIVO; INFLAMMATION; ANTIGEN; ASTHMA; DIFFERENTIATION; HOMEOSTASIS;
D O I
10.1371/journal.pone.0053242
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Conventional dendritic cells (DCs) are considered to be the prime initiators of airway allergy. Yet, it remains unclear whether specific DC subsets are preferentially involved in allergic airway sensitization. Here, we systematically assessed the respective pro-allergic potential of individually sorted lung DC subsets isolated from house dust mite antigen (HDM)-treated donor mice, following transfer to naive recipients. Transfer of lung CD11c(+)CD11b(+) DCs, but not CD11c(+)CD11b(-)CD103(+) DCs, was sufficient to prime airway allergy. The CD11c(+)CD11b(+) DC subpopulation was composed of CD11c(+)CD11b(+)Ly6C(+) inflammatory monocyte-derived cells, whose numbers increase in the lungs following HDM exposure, and of CD11c(+)CD11b(+)Ly6C(-) DCs, which remain stable. Counterintuitively, only CD11c(+)CD11b(+)Ly6C(-) DCs, and not CD11c(+)CD11b(+)Ly6C(+) DCs, were able to convey antigen to the lymph nodes and induce adaptive T cell responses and subsequent airway allergy. Our results thus support that lung resident non-inflammatory CD11c(+)CD11b(+)Ly6C(-) DCs are the essential inducers of allergic airway sensitization to the common aeroallergen HDM in mice.
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页数:12
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