Abstract
We analyzed the autologous NK cell interaction with gliadin-presenting dendritic cells. Gliadin is the known Ag priming the celiac disease (CD) pathogenesis. We demonstrate that gliadin prevents immature dendritic cells (iDCs) elimination by NK cells. Furthermore, cooperation between human NK cells-iDCs and T cells increases IFN-γ production of anti-gliadin immune response. Gliadin fractions were analyzed for their capability to stabilize HLA-E molecules. The α and ω fractions conferred the protection from NK cell lysis to iDCs and increased their HLA-E expression. Gliadin pancreatic enzyme digest and a peptide derived from gliadin a increased HLA-E levels on murine RMA-S/HLA-E-transfected cells. Analysis of HLA-E expression in the small intestinal mucosa of gluten-containing diet celiac patients and organ culture experiments confirmed the in vitro data.
| Original language | English |
|---|---|
| Pages (from-to) | 372-381 |
| Number of pages | 10 |
| Journal | Journal of Immunology |
| Volume | 179 |
| Issue number | 1 |
| Publication status | Published - Jul 1 2007 |
Fingerprint
ASJC Scopus subject areas
- Immunology
Cite this
Gliadin regulates the NK-dendritic cell cross-talk by HLA-E surface stabilization. / Terrazzano, Giuseppe; Sica, Michela; Gianfrani, Carmen; Mazzarella, Giuseppe; Maurano, Francesco; De Giulio, Beatrice; De Saint-Mezard, Sophie; Zanzi, Delia; Maiuri, Luigi; Londei, Marco; Jabri, Bana; Troncone, Riccardo; Auricchio, Salvatore; Zappacosta, Serafino; Carbone, Ennio.
In: Journal of Immunology, Vol. 179, No. 1, 01.07.2007, p. 372-381.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Gliadin regulates the NK-dendritic cell cross-talk by HLA-E surface stabilization
AU - Terrazzano, Giuseppe
AU - Sica, Michela
AU - Gianfrani, Carmen
AU - Mazzarella, Giuseppe
AU - Maurano, Francesco
AU - De Giulio, Beatrice
AU - De Saint-Mezard, Sophie
AU - Zanzi, Delia
AU - Maiuri, Luigi
AU - Londei, Marco
AU - Jabri, Bana
AU - Troncone, Riccardo
AU - Auricchio, Salvatore
AU - Zappacosta, Serafino
AU - Carbone, Ennio
PY - 2007/7/1
Y1 - 2007/7/1
N2 - We analyzed the autologous NK cell interaction with gliadin-presenting dendritic cells. Gliadin is the known Ag priming the celiac disease (CD) pathogenesis. We demonstrate that gliadin prevents immature dendritic cells (iDCs) elimination by NK cells. Furthermore, cooperation between human NK cells-iDCs and T cells increases IFN-γ production of anti-gliadin immune response. Gliadin fractions were analyzed for their capability to stabilize HLA-E molecules. The α and ω fractions conferred the protection from NK cell lysis to iDCs and increased their HLA-E expression. Gliadin pancreatic enzyme digest and a peptide derived from gliadin a increased HLA-E levels on murine RMA-S/HLA-E-transfected cells. Analysis of HLA-E expression in the small intestinal mucosa of gluten-containing diet celiac patients and organ culture experiments confirmed the in vitro data.
AB - We analyzed the autologous NK cell interaction with gliadin-presenting dendritic cells. Gliadin is the known Ag priming the celiac disease (CD) pathogenesis. We demonstrate that gliadin prevents immature dendritic cells (iDCs) elimination by NK cells. Furthermore, cooperation between human NK cells-iDCs and T cells increases IFN-γ production of anti-gliadin immune response. Gliadin fractions were analyzed for their capability to stabilize HLA-E molecules. The α and ω fractions conferred the protection from NK cell lysis to iDCs and increased their HLA-E expression. Gliadin pancreatic enzyme digest and a peptide derived from gliadin a increased HLA-E levels on murine RMA-S/HLA-E-transfected cells. Analysis of HLA-E expression in the small intestinal mucosa of gluten-containing diet celiac patients and organ culture experiments confirmed the in vitro data.
UR - http://www.scopus.com/inward/record.url?scp=34250807802&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34250807802&partnerID=8YFLogxK
M3 - Article
C2 - 17579058
AN - SCOPUS:34250807802
VL - 179
SP - 372
EP - 381
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 1
ER -