AID-expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway

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dc.contributor.author	Pérez García, Arantxa
dc.contributor.author	Pérez Durán, Pablo
dc.contributor.author	Wossning, Thomas
dc.contributor.author	Sernandez, Isora V.
dc.contributor.author	Mur, Sonia M.
dc.contributor.author	Cañamero, Marta
dc.contributor.author	Real, Francisco X.
dc.contributor.author	Ramiro, Almudena R.
dc.date	2015
dc.identifier.citation	Pérez-García A, Pérez-Durán P, Wossning T, Sernandez IV, Mur SM, Cañamero M et al. AID-expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway. EMBO molecular medicine. 2015; 7(10): 1327-1336. DOI 10.15252/emmm.201505348
dc.identifier.citation	1757-4676
dc.identifier.citation	http://dx.doi.org/10.15252/emmm.201505348.
dc.identifier.uri	http://hdl.handle.net/10230/26172
dc.format	application/pdf
dc.language.iso	eng
dc.publisher	Wiley-Blackwell
dc.relation	EMBO molecular medicine. 2015; 7(10): 1327-1336
dc.rights	© 2015 The Authors. Published under the terms of the CC BY 4.0 license
dc.rights	https://creativecommons.org/licenses/by/4.0/
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	Pàncrees -- Càncer
dc.subject	Epiteli -- Càncer
dc.subject	NKG2D
dc.subject	Activation‐induced deaminase
dc.subject	Cancer
dc.subject	Epithelium
dc.subject	Pancreas
dc.title	AID-expressing epithelium is protected from oncogenic transformation by an NKG2D surveillance pathway
dc.type	info:eu-repo/semantics/article
dc.type	info:eu-repo/semantics/publishedVersion
dc.description.abstract	Activation-induced deaminase (AID) initiates secondary antibody diversification in germinal center B cells, giving rise to higher affinity antibodies through somatic hypermutation (SHM) or to isotype-switched antibodies through class switch recombination (CSR). SHM and CSR are triggered by AID-mediated deamination of cytosines in immunoglobulin genes. Importantly, AID activity in B cells is not restricted to Ig loci and can promote mutations and pro-lymphomagenic translocations, establishing a direct oncogenic mechanism for germinal center-derived neoplasias. AID is also expressed in response to inflammatory cues in epithelial cells, raising the possibility that AID mutagenic activity might drive carcinoma development. We directly tested this hypothesis by generating conditional knock-in mouse models for AID overexpression in colon and pancreas epithelium. AID overexpression alone was not sufficient to promote epithelial cell neoplasia in these tissues, in spite of displaying mutagenic and genotoxic activity. Instead, we found that heterologous AID expression in pancreas promotes the expression of NKG2D ligands, the recruitment of CD8(+) T cells, and the induction of epithelial cell death. Our results indicate that AID oncogenic potential in epithelial cells can be neutralized by immunosurveillance protective mechanisms.
dc.description.abstract	AP‐G is a fellow of the research training program (FPU‐ AP2009‐1732) funded by the Ministerio de Educación, Cultura y Deporte, PP‐D was an FPI fellow from the Ministerio de Ciencia e Innovación. ARR is supported by Centro Nacional de Investigaciones Cardiovaculares (CNIC). This work was funded by grants from the Ministerio de Economía y Competitividad (SAF2010‐21394, SAF2013‐42767‐R) and the European Research Council Starting Grant program (BCLYM‐207844) to ARR. The CNIC is supported by the Ministerio de Economía y Competitividad and the Pro‐CNIC Foundation. FXR is supported by SAF2011‐29530 and ONCOBIO Consolider grants from Ministerio de Economía y Competitividad (Madrid, Spain), RTICC from Instituto de Salud Carlos III, and grant 256974 from European Union Seventh Framework Programme to FXR.

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