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

By S. Hüe, Jean-Jacques Mention, R. Monteiro, Shaoling Zhang, C. Cellier, J. Schmitz, V. Verkarre, Nassima Fodil, S. Bahram, N. Cerf‐Bensussan and 1 more. Immunity, 2004

775 citations recorded by the source corpus.

Subfields: Gastroenterology, Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/2826e9d5c69a2b02fae1e434bc48026e2df5b4d7

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In Immunology

1. S. Gasser
2. W. Deng
3. Heiyoun Jung
4. Benjamin G. Gowen
5. D. Raulet

Citations in the corpus

• Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4 (2012, background): “…from -gliadin that lack adaptive stimulatory capacity were incriminated as triggers of innate immunity as they induced IL-15 and Cox-2 expression in patients’ biopsies (Maiuri et al., 2003) and MHC class I polypeptide–related sequence A (MICA) on intestinal epithelial cells (Hüe et al., 2004).”
• Regulation of ligands for the NKG2D activating receptor (2013, background): “Furthermore, NKG2D was not appreciably downregulated on cells in patients with rheumatoid arthritis or celiac disease (131, 132) or in mice with a ubiquitously expressed MICA transgene (130), all of which have high levels of serum MICA.”