Absence of ATM leads to altered NK cell function in mice

Copyright © 2024 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 263(2024) vom: 22. Juni, Seite 110233
1. Verfasser: Covino, Daniela Angela (VerfasserIn)
Weitere Verfasser: Desimio, Maria Giovanna, Giovinazzo, Alessandro, de Oliveira, Bruna Sabino Pinho, Merolle, Matilde, Marazziti, Daniela, Pellegrini, Manuela, Doria, Margherita
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2024
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article ATM kinase Ataxia-telangiectasia Cytotoxicity H60 MULT1 NKG2D Natural killer cells RAE-1 TNF-α mehr... Klrk1 protein, mouse Atm protein, mouse UL16 binding protein 1, mouse
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245 1 0 |a Absence of ATM leads to altered NK cell function in mice 
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520 |a Ataxia-telangiectasia (A-T) is a rare disorder caused by genetic defects of A-T mutated (ATM) kinase, a key regulator of stress response, and characterized by neurodegeneration, immunodeficiency, and high incidence of cancer. Here we investigated NK cells in a mouse model of A-T (Atm-/-) showing that they are strongly impaired at killing tumor cells due to a block of early signaling events. On the other hand, in Atm-/- littermates with thymic lymphoma NK cell cytotoxicity is enhanced as compared with ATM-proficient mice, possibly via tumor-produced TNF-α. Results also suggest that expansion of exhausted NKG2D+ NK cells in Atm-/- mice is driven by low-level expression of stress-inducible NKG2D ligands, whereas development of thymoma expressing the high-affinity MULT1 ligand is associated with NKG2D down-regulation on NK cells. These results expand our understanding of immunodeficiency in A-T and encourage exploring NK cell biology in A-T patients in the attempt to identify cancer predictive biomarkers and novel therapeutic targets 
650 4 |a Journal Article 
650 4 |a ATM kinase 
650 4 |a Ataxia-telangiectasia 
650 4 |a Cytotoxicity 
650 4 |a H60 
650 4 |a MULT1 
650 4 |a NKG2D 
650 4 |a Natural killer cells 
650 4 |a RAE-1 
650 4 |a TNF-α 
650 7 |a Klrk1 protein, mouse  |2 NLM 
650 7 |a Atm protein, mouse  |2 NLM 
650 7 |a UL16 binding protein 1, mouse  |2 NLM 
700 1 |a Desimio, Maria Giovanna  |e verfasserin  |4 aut 
700 1 |a Giovinazzo, Alessandro  |e verfasserin  |4 aut 
700 1 |a de Oliveira, Bruna Sabino Pinho  |e verfasserin  |4 aut 
700 1 |a Merolle, Matilde  |e verfasserin  |4 aut 
700 1 |a Marazziti, Daniela  |e verfasserin  |4 aut 
700 1 |a Pellegrini, Manuela  |e verfasserin  |4 aut 
700 1 |a Doria, Margherita  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Clinical immunology (Orlando, Fla.)  |d 1999  |g 263(2024) vom: 22. Juni, Seite 110233  |w (DE-627)NLM098196855  |x 1521-7035  |7 nnns 
773 1 8 |g volume:263  |g year:2024  |g day:22  |g month:06  |g pages:110233 
856 4 0 |u http://dx.doi.org/10.1016/j.clim.2024.110233  |3 Volltext 
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