A direct role for NKG2D/MICA interaction in villous atrophy during celiac disease

被引:543
作者
Hüe, S
Mention, JJ
Monteiro, RC
Zhang, SL
Cellier, C
Schmitz, J
Verkarre, V
Fodil, N
Bahram, S
Cerf-Bensussan, N
Caillat-Zucman, S [1 ]
机构
[1] Hop Necker Enfants Malad, INSERM, Equipe Avenir, F-75015 Paris, France
[2] Hop Necker Enfants Malad, INSERM, EMI 0212, F-75015 Paris, France
[3] Hop Necker Enfants Malad, Serv Gastroenterol Pediat, F-75015 Paris, France
[4] Fac Bichat, INSERM, E0225, F-75018 Paris, France
[5] Hop Europeen Georges Pompidou, Dept Hepatogastroenterol, F-75015 Paris, France
[6] Ctr Rech Immunol & Hematol, INSERM, CreS, F-67000 Strasbourg, France
关键词
D O I
10.1016/j.immuni.2004.06.018
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
MICA molecules interact with the NKG2D-activating receptor on human NK and CD8 T cells. We investigated the participation of the MICA/NKG2D pathway in the destruction of intestinal epithelium by intraepithelial T lymphocytes (IEL) in Celiac disease and its premalignant complication, refractory sprue. We show that MICA is strongly expressed at epithelial cell surface in patients with active disease and is induced by gliadin or its p31-49 derived peptide upon in vitro challenge, an effect relayed by IL-15. This triggers direct activation and costimulation of IEL through engagement of NKG2D, leading to an innate-like cytotoxicity toward epithelial targets and enhanced TCR-dependent CD8 T cell-mediated adaptive response. Villous atrophy in Celiac disease might thus be ascribed to an IEL-medlated damage to enterocytes involving NKG2D/MICA interaction after gliadin-induced expression of MICA on gut epithelium. This supports a key role for MIC/NKG2D in the activation of intraepithelial immunity in response to danger.
引用
收藏
页码:367 / 377
页数:11
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