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A Direct Role for NKG2D/MICA Interaction in Villous Atrophy during Celiac Disease
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...
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| Published in: | Immunity (Cambridge, Mass.) Mass.), 2004-09, Vol.21 (3), p.367-377 |
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| Main Authors: | , , , , , , , , , , |
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| cites | cdi_FETCH-LOGICAL-c529t-a1068baaf6d2be28eef0a36c3929692403fd7a8ddfc42fac751b9f8d69752be73 |
| container_end_page | 377 |
| container_issue | 3 |
| container_start_page | 367 |
| container_title | Immunity (Cambridge, Mass.) |
| container_volume | 21 |
| creator | Hüe, Sophie Mention, Jean-Jacques Monteiro, Renato C. Zhang, ShaoLing Cellier, Christophe Schmitz, Jacques Verkarre, Virginie Fodil, Nassima Bahram, Seiamak Cerf-Bensussan, Nadine Caillat-Zucman, Sophie |
| description | 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-mediated 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. |
| doi_str_mv | 10.1016/j.immuni.2004.06.018 |
| format | article |
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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-mediated 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.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2004.06.018</identifier><identifier>PMID: 15357948</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Atrophy - immunology ; Atrophy - pathology ; Celiac disease ; Celiac Disease - blood ; Celiac Disease - immunology ; Celiac Disease - pathology ; Cytotoxicity Tests, Immunologic ; Enterocytes - immunology ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Gliadin - pharmacology ; Gluten ; HeLa Cells ; Humans ; Immunohistochemistry ; Interleukin-15 - immunology ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - immunology ; Intestinal Mucosa - metabolism ; Intestine, Small - immunology ; Intestine, Small - pathology ; Lymphocytes ; NK Cell Lectin-Like Receptor Subfamily K ; Protein Biosynthesis ; Proteins - drug effects ; Proteins - immunology ; Receptors, Immunologic - immunology ; Receptors, Natural Killer Cell ; RNA, Long Noncoding ; RNA, Untranslated ; Rodents ; Small intestine ; T-Lymphocytes - immunology</subject><ispartof>Immunity (Cambridge, Mass.), 2004-09, Vol.21 (3), p.367-377</ispartof><rights>2004 Cell Press</rights><rights>Copyright Elsevier Limited Sep 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c529t-a1068baaf6d2be28eef0a36c3929692403fd7a8ddfc42fac751b9f8d69752be73</citedby><cites>FETCH-LOGICAL-c529t-a1068baaf6d2be28eef0a36c3929692403fd7a8ddfc42fac751b9f8d69752be73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15357948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hüe, Sophie</creatorcontrib><creatorcontrib>Mention, Jean-Jacques</creatorcontrib><creatorcontrib>Monteiro, Renato C.</creatorcontrib><creatorcontrib>Zhang, ShaoLing</creatorcontrib><creatorcontrib>Cellier, Christophe</creatorcontrib><creatorcontrib>Schmitz, Jacques</creatorcontrib><creatorcontrib>Verkarre, Virginie</creatorcontrib><creatorcontrib>Fodil, Nassima</creatorcontrib><creatorcontrib>Bahram, Seiamak</creatorcontrib><creatorcontrib>Cerf-Bensussan, Nadine</creatorcontrib><creatorcontrib>Caillat-Zucman, Sophie</creatorcontrib><title>A Direct Role for NKG2D/MICA Interaction in Villous Atrophy during Celiac Disease</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>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-mediated 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.</description><subject>Atrophy - immunology</subject><subject>Atrophy - pathology</subject><subject>Celiac disease</subject><subject>Celiac Disease - blood</subject><subject>Celiac Disease - immunology</subject><subject>Celiac Disease - pathology</subject><subject>Cytotoxicity Tests, Immunologic</subject><subject>Enterocytes - immunology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Flow Cytometry</subject><subject>Gliadin - pharmacology</subject><subject>Gluten</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Interleukin-15 - immunology</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Intestinal Mucosa - immunology</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestine, Small - immunology</subject><subject>Intestine, Small - pathology</subject><subject>Lymphocytes</subject><subject>NK Cell Lectin-Like Receptor Subfamily K</subject><subject>Protein Biosynthesis</subject><subject>Proteins - drug effects</subject><subject>Proteins - immunology</subject><subject>Receptors, Immunologic - immunology</subject><subject>Receptors, Natural Killer Cell</subject><subject>RNA, Long Noncoding</subject><subject>RNA, Untranslated</subject><subject>Rodents</subject><subject>Small intestine</subject><subject>T-Lymphocytes - immunology</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNp9kF1rFDEUhoMotlb_gUhA8G6m-ZpkciMsW63FVlHU25BNTjTLzGSbzAj992bdhUIvenXOxfO-5_Ag9JqSlhIqz7dtHMdlii0jRLREtoT2T9ApJVo1gvbk6X5XolGS8hP0opQtIVR0mjxHJ7TjndKiP0XfVvgiZnAz_p4GwCFl_OXzJbs4v7lar_DVNEO2bo5pwnHCv-IwpKXg1ZzT7s8d9kuO02-8hiFaV3sK2AIv0bNghwKvjvMM_fz44cf6U3P99bJ2XjeuY3puLCWy31gbpGcbYD1AIJZLxzXTUjNBePDK9t4HJ1iwTnV0o0PvpVZdDSh-ht4denc53S5QZjPG4mAY7AT1SVMVcM3VHnz7ANymJU_1N0M7IhhTnLNKiQPlciolQzC7HEeb7wwlZi_cbM1BuNkLN0SaKrzG3hzLl80I_j50NFyB9wcAqou_EbIpLsLkwP_XbnyKj1_4B1vrkbI</recordid><startdate>20040901</startdate><enddate>20040901</enddate><creator>Hüe, Sophie</creator><creator>Mention, Jean-Jacques</creator><creator>Monteiro, Renato C.</creator><creator>Zhang, ShaoLing</creator><creator>Cellier, Christophe</creator><creator>Schmitz, Jacques</creator><creator>Verkarre, Virginie</creator><creator>Fodil, Nassima</creator><creator>Bahram, Seiamak</creator><creator>Cerf-Bensussan, Nadine</creator><creator>Caillat-Zucman, Sophie</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20040901</creationdate><title>A Direct Role for NKG2D/MICA Interaction in Villous Atrophy during Celiac Disease</title><author>Hüe, Sophie ; 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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-mediated 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.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15357948</pmid><doi>10.1016/j.immuni.2004.06.018</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Atrophy - immunology Atrophy - pathology Celiac disease Celiac Disease - blood Celiac Disease - immunology Celiac Disease - pathology Cytotoxicity Tests, Immunologic Enterocytes - immunology Enzyme-Linked Immunosorbent Assay Flow Cytometry Gliadin - pharmacology Gluten HeLa Cells Humans Immunohistochemistry Interleukin-15 - immunology Intestinal Mucosa - drug effects Intestinal Mucosa - immunology Intestinal Mucosa - metabolism Intestine, Small - immunology Intestine, Small - pathology Lymphocytes NK Cell Lectin-Like Receptor Subfamily K Protein Biosynthesis Proteins - drug effects Proteins - immunology Receptors, Immunologic - immunology Receptors, Natural Killer Cell RNA, Long Noncoding RNA, Untranslated Rodents Small intestine T-Lymphocytes - immunology |
| title | A Direct Role for NKG2D/MICA Interaction in Villous Atrophy during Celiac Disease |
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