Tumorigenic adenovirus 12 cells evade NK cell lysis by reducing the expression of NKG2D ligands

Christa Y. Heyward; Rajen Patel; Emily M. Mace; Jennifer T. Grier; Hancheng Guan; Andrew P. Makrigiannis; Jordan S. Orange; Robert P. Ricciardi

doi:10.1016/j.imlet.2012.03.001

Tumorigenic adenovirus 12 cells evade NK cell lysis by reducing the expression of NKG2D ligands

Christa Y. Heyward, Rajen Patel, Emily M. Mace, Jennifer T. Grier, Hancheng Guan, Andrew P. Makrigiannis, Jordan S. Orange, Robert P. Ricciardi

Research output: Contribution to journal › Article › peer-review

4 Citations (Scopus)

Abstract

Activation of natural killer (NK) cells depends on a balance between signals received from activation and inhibitory ligands expressed on the surface of target cells. Tumorigenic human adenovirus 12 (Ad12) transformed cells express low levels of the NK cell inhibitory ligand MHC I, but do not exhibit increased sensitivity to NK cell lysis compared to their non-tumorigenic counterparts. Analysis of the expression of activation ligands that bind to the NKG2D receptor revealed that RAE1β and H60 were reduced on the surface of Ad12 mouse cells as well as at the level of transcription. In accord with these results, RAE1 localization to the synapse and sensitivity to NK cell cytotoxicity were also diminished. The reduced transcription of the rat NKG2D ligands, RAEt1L and RRTL, in tumorigenic rat cells compared to non-tumorigenic counterparts implies that both mouse and rat cell lines share a common mechanism of NKG2D ligand activation subverted by Ad12.

Original language	English
Pages (from-to)	16-23
Number of pages	8
Journal	Immunology Letters
Volume	144
Issue number	1-2
DOIs	https://doi.org/10.1016/j.imlet.2012.03.001
Publication status	Published - May 30 2012
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by grant CA29797 from the National Caner Institute (to R.P.R). and the NIH training grant in Virology 5-T32-AI-007324-16 (to C.Y.H.).

ASJC Scopus Subject Areas

Immunology and Allergy
Immunology

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10.1016/j.imlet.2012.03.001

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title = "Tumorigenic adenovirus 12 cells evade NK cell lysis by reducing the expression of NKG2D ligands",

abstract = "Activation of natural killer (NK) cells depends on a balance between signals received from activation and inhibitory ligands expressed on the surface of target cells. Tumorigenic human adenovirus 12 (Ad12) transformed cells express low levels of the NK cell inhibitory ligand MHC I, but do not exhibit increased sensitivity to NK cell lysis compared to their non-tumorigenic counterparts. Analysis of the expression of activation ligands that bind to the NKG2D receptor revealed that RAE1β and H60 were reduced on the surface of Ad12 mouse cells as well as at the level of transcription. In accord with these results, RAE1 localization to the synapse and sensitivity to NK cell cytotoxicity were also diminished. The reduced transcription of the rat NKG2D ligands, RAEt1L and RRTL, in tumorigenic rat cells compared to non-tumorigenic counterparts implies that both mouse and rat cell lines share a common mechanism of NKG2D ligand activation subverted by Ad12.",

author = "Heyward, {Christa Y.} and Rajen Patel and Mace, {Emily M.} and Grier, {Jennifer T.} and Hancheng Guan and Makrigiannis, {Andrew P.} and Orange, {Jordan S.} and Ricciardi, {Robert P.}",

note = "Funding Information: This work was supported by grant CA29797 from the National Caner Institute (to R.P.R). and the NIH training grant in Virology 5-T32-AI-007324-16 (to C.Y.H.).",

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doi = "10.1016/j.imlet.2012.03.001",

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AU - Heyward, Christa Y.

AU - Patel, Rajen

AU - Mace, Emily M.

AU - Grier, Jennifer T.

AU - Guan, Hancheng

AU - Makrigiannis, Andrew P.

AU - Orange, Jordan S.

AU - Ricciardi, Robert P.

N1 - Funding Information: This work was supported by grant CA29797 from the National Caner Institute (to R.P.R). and the NIH training grant in Virology 5-T32-AI-007324-16 (to C.Y.H.).

PY - 2012/5/30

Y1 - 2012/5/30

N2 - Activation of natural killer (NK) cells depends on a balance between signals received from activation and inhibitory ligands expressed on the surface of target cells. Tumorigenic human adenovirus 12 (Ad12) transformed cells express low levels of the NK cell inhibitory ligand MHC I, but do not exhibit increased sensitivity to NK cell lysis compared to their non-tumorigenic counterparts. Analysis of the expression of activation ligands that bind to the NKG2D receptor revealed that RAE1β and H60 were reduced on the surface of Ad12 mouse cells as well as at the level of transcription. In accord with these results, RAE1 localization to the synapse and sensitivity to NK cell cytotoxicity were also diminished. The reduced transcription of the rat NKG2D ligands, RAEt1L and RRTL, in tumorigenic rat cells compared to non-tumorigenic counterparts implies that both mouse and rat cell lines share a common mechanism of NKG2D ligand activation subverted by Ad12.

AB - Activation of natural killer (NK) cells depends on a balance between signals received from activation and inhibitory ligands expressed on the surface of target cells. Tumorigenic human adenovirus 12 (Ad12) transformed cells express low levels of the NK cell inhibitory ligand MHC I, but do not exhibit increased sensitivity to NK cell lysis compared to their non-tumorigenic counterparts. Analysis of the expression of activation ligands that bind to the NKG2D receptor revealed that RAE1β and H60 were reduced on the surface of Ad12 mouse cells as well as at the level of transcription. In accord with these results, RAE1 localization to the synapse and sensitivity to NK cell cytotoxicity were also diminished. The reduced transcription of the rat NKG2D ligands, RAEt1L and RRTL, in tumorigenic rat cells compared to non-tumorigenic counterparts implies that both mouse and rat cell lines share a common mechanism of NKG2D ligand activation subverted by Ad12.

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Tumorigenic adenovirus 12 cells evade NK cell lysis by reducing the expression of NKG2D ligands

Abstract

Bibliographical note

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