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Mouse Cytomegalovirus m153 Protein Stabilizes Expression of the Inhibitory NKR-P1B Ligand Clr-b
Journal of Virology, 94 (2019), 1; e01220-19. https://doi.org/10.1128/JVI.01220-19
Aguilar, Oscar A.; Sampaio, Isabella S.; Rahim, Mir Munir A.; Samaniego, Jackeline D.; Tilahun, Mulualem E.; Krishnamoorthy, Mithunah; Popović, Branka; Babić, Marina; Krmpotić, Astrid; Treanor, Bebhinn; Margulies, David H.; Allan, David S.J.; Makrigiannis, Andrew P.; Jonjić, Stipan; Carlyle, James R. Više autora...

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Aguilar, O. A., Sampaio, I. S., Rahim, M. M. A., Samaniego, J. D., Tilahun, M. E., Krishnamoorthy, M. ... Carlyle, J. R. (2019). Mouse Cytomegalovirus m153 Protein Stabilizes Expression of the Inhibitory NKR-P1B Ligand Clr-b. Journal of Virology, 94. (1). doi: 10.1128/JVI.01220-19

Aguilar, Oscar A., et al. "Mouse Cytomegalovirus m153 Protein Stabilizes Expression of the Inhibitory NKR-P1B Ligand Clr-b." Journal of Virology, vol. 94, br. 1, 2019. https://doi.org/10.1128/JVI.01220-19

Aguilar, Oscar A., Isabella S. Sampaio, Mir Munir A. Rahim, Jackeline D. Samaniego, Mulualem E. Tilahun, Mithunah Krishnamoorthy, Branka Popović, et al. "Mouse Cytomegalovirus m153 Protein Stabilizes Expression of the Inhibitory NKR-P1B Ligand Clr-b." Journal of Virology 94, br. 1 (2019). https://doi.org/10.1128/JVI.01220-19

Aguilar, O. A., et al. (2019) 'Mouse Cytomegalovirus m153 Protein Stabilizes Expression of the Inhibitory NKR-P1B Ligand Clr-b', Journal of Virology, 94(1). doi: 10.1128/JVI.01220-19

Aguilar OA, Sampaio IS, Rahim MMA, Samaniego JD, Tilahun ME, Krishnamoorthy M, i sur.. Mouse Cytomegalovirus m153 Protein Stabilizes Expression of the Inhibitory NKR-P1B Ligand Clr-b. Journal of Virology [Internet]. 12.12.2019. [pristupljeno 15.04.2025.];94(1). doi: 10.1128/JVI.01220-19

O. A. Aguilar, et al., "Mouse Cytomegalovirus m153 Protein Stabilizes Expression of the Inhibitory NKR-P1B Ligand Clr-b", Journal of Virology, vol. 94, br. 1, Prosinac 2019. [Online]. Dostupno na: https://urn.nsk.hr/urn:nbn:hr:184:634217. [Citirano: 15.04.2025.]

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Naslov (engleski)Mouse Cytomegalovirus m153 Protein Stabilizes Expression of the Inhibitory NKR-P1B Ligand Clr-b
AutorOscar A. Aguilar
AutorIsabella S. Sampaio
AutorMir Munir A. Rahim
AutorJackeline D. Samaniego
AutorMulualem E. Tilahun
AutorMithunah Krishnamoorthy
AutorBranka Popović
AutorMarina Babić
AutorAstrid Krmpotić
AutorBebhinn Treanor
AutorDavid H. Margulies
AutorDavid S.J. Allan
AutorAndrew P. Makrigiannis
AutorStipan Jonjić
AutorJames R. Carlyle
Autorova ustanovaSveučilište u Rijeci
Medicinski fakultet
(Katedra za histologiju i embriologiju)
Znanstveno / umjetničko
područje, polje i grana		BIOMEDICINA I ZDRAVSTVO
Temeljne medicinske znanosti
Sažetak (engleski)
ABSTRACT Natural killer (NK) cells are a subset of innate lymphoid cells (ILC) capable of recognizing stressed and infected cells through multiple germ line-encoded receptor-ligand interactions. Missing-self recognition involves NK cell sensing of the loss of host-encoded inhibitory ligands on target cells, including MHC class I (MHC-I) molecules and other MHC-I-independent ligands. Mouse cytomegalovirus (MCMV) infection promotes a rapid host-mediated loss of the inhibitory... Više NKR-P1B ligand Clr-b (encoded by ) on infected cells. Here we provide evidence that an MCMV m145 family member, m153, functions to stabilize cell surface Clr-b during MCMV infection. Ectopic expression of m153 in fibroblasts augments Clr-b cell surface levels. Moreover, infections using -deficient MCMV mutants (Δm144-m158 and Δm153) show an accelerated and exacerbated Clr-b downregulation. Importantly, enhanced loss of Clr-b during Δm153 mutant infection reverts to wild-type levels upon exogenous m153 complementation in fibroblasts. While the effects of m153 on Clr-b levels are independent of transcription, imaging experiments revealed that the m153 and Clr-b proteins only minimally colocalize within the same subcellular compartments, and tagged versions of the proteins were refractory to coimmunoprecipitation under mild-detergent conditions. Surprisingly, the Δm153 mutant possesses enhanced virulence , independent of both Clr-b and NKR-P1B, suggesting that m153 potentially targets additional host factors. Nevertheless, the present data highlight a unique mechanism by which MCMV modulates NK ligand expression. Cytomegaloviruses are betaherpesviruses that in immunocompromised individuals can lead to severe pathologies. These viruses encode various gene products that serve to evade innate immune recognition. NK cells are among the first immune cells that respond to CMV infection and use germ line-encoded NK cell receptors (NKR) to distinguish healthy from virus-infected cells. One such axis that plays a critical role in NK recognition involves the inhibitory NKR-P1B receptor, which engages the host ligand Clr-b, a molecule commonly lost on stressed cells (“missing-self”). In this study, we discovered that mouse CMV utilizes the m153 glycoprotein to circumvent host-mediated Clr-b downregulation, in order to evade NK recognition. These results highlight a novel MCMV-mediated immune evasion strategy. Sakrij dio sažetka
Ključne riječi (engleski)
Jezikengleski
Vrsta publikacijeZnanstveni rad - Izvorni znanstveni rad
Status objaveObjavljen
Vrsta recenzijeRecenziran - međunarodna recenzija
Verzija publikacijeObjavljena verzija rada (izdavačev PDF)
Naslov časopisaJournal of Virology
Brojčani podacivol. 94, br. 1, e01220-19
p-ISSN0022-538X
e-ISSN1098-5514
DOIhttps://doi.org/10.1128/JVI.01220-19
URN:NBNurn:nbn:hr:184:634217
Datum objave publikacije2019-12-12
ProjektŠifra: N/A
Naziv (hrvatski): Centar izvrsnosti za virusnu imunologiju i cjepiva
Kratica: CERVirVac
Voditelj: Stipan Jonjić
Pravna nadležnost: Hrvatska
Financijer: MZOS
Linija financiranja: ZCI
ProjektŠifra: KK.011.1.01.0006
Naziv (engleski): Jačanje kapaciteta CerVirVac-a za istraživanja u virusnoj imunologiji i vakcinologiji
Voditelj: Stipan Jonjić
Pravna nadležnost: eu
Financijer: ERDF
URL dokumentahttps://jvi.asm.org/content/94/1/e01220-19
Vrsta resursaTekst
Prava pristupaOtvoreni pristup
Uvjeti korištenjaIkona licence Imenovanje-Nekomercijalno-Bez prerada 4.0 međunarodna (CC BY-NC-ND 4.0)
Datum i vrijeme pohrane2020-11-24 18:08:48
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