scholarly journals Crk Adaptor Proteins Regulate NK Cell Expansion and Differentiation during Mouse Cytomegalovirus Infection

2018 ◽  
Vol 200 (10) ◽  
pp. 3420-3428 ◽  
Author(s):  
Tsukasa Nabekura ◽  
Zhiying Chen ◽  
Casey Schroeder ◽  
Taeju Park ◽  
Eric Vivier ◽  
...  
Keyword(s):  
Cell Expansion ◽  
Cytomegalovirus Infection ◽  
Nk Cell ◽  
Adaptor Proteins ◽  
Mouse Cytomegalovirus

scholarly journals Mouse Ly49G2+ NK cells dominate early responses during both immune reconstitution and activation independently of MHC

Blood ◽  
2011 ◽  
Vol 117 (26) ◽  
pp. 7032-7041 ◽  
Author(s):  
Isabel Barao ◽  
Maite Alvarez ◽  
Erik Ames ◽  
Mark T. Orr ◽  
Heather E. Stefanski ◽  
...  
Keyword(s):  
Nk Cells ◽  
Mhc Class I ◽  
Cytomegalovirus Infection ◽  
Immune Reconstitution ◽  
Nk Cell ◽  
Rapid Expansion ◽  
Normal Pattern ◽  
Mouse Cytomegalovirus ◽  
Single Positive ◽  
Independent Expansion

Abstract Natural killer (NK) cell subsets can be defined by the differential expression of inhibitory receptors for MHC class I molecules. Early after congenic HSCT, we found that Ly49G2high single-positive NK cells repopulated, displayed an activated phenotype, and were highly cytolytic. Over time, this subset was replaced with NK cells with a normal pattern of Ly49 expression. Treatment of mice with IL-2 also resulted in the rapid expansion of these Ly49G2high single-positive NK cells. Only the Ly49g (Klra7) Pro1 transcript was highly induced in both HSCT- and IL-2–treated recipients. MHC-independent expansion of the Ly49G2+ subset was also observed after Listeria monocytogenes or mouse cytomegalovirus infection. Our data indicate that during reconstitution after HSCT and various activation stimuli, Ly49G2+ NK cells represent the “first-responder” NK cells, which occur independently of NK-cell licensing via Ly49-MHC interactions. These data suggest that the inhibitory Ly49G2 receptor represents an activation marker on mouse NK cells under various conditions.

scholarly journals Ly49C Impairs NK Cell Memory in Mouse Cytomegalovirus Infection

2016 ◽  
Vol 197 (1) ◽  
pp. 128-140 ◽  
Author(s):  
Catherine A. Forbes ◽  
Anthony A. Scalzo ◽  
Mariapia A. Degli-Esposti ◽  
Jerome D. Coudert
Keyword(s):  
Cytomegalovirus Infection ◽  
Nk Cell ◽  
Mouse Cytomegalovirus ◽  
Cell Memory

scholarly journals Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection

2017 ◽  
Vol 199 (5) ◽  
pp. 1567-1571 ◽  
Author(s):  
Tsukasa Nabekura ◽  
Dagmar Gotthardt ◽  
Kouta Niizuma ◽  
Tihana Trsan ◽  
Tina Jenus ◽  
...  
Keyword(s):  
Cytomegalovirus Infection ◽  
Nk Cell ◽  
Cutting Edge ◽  
Mouse Cytomegalovirus ◽  
Cell Responses

scholarly journals Intrinsic Contribution of Perforin to NK-Cell Homeostasis during Mouse Cytomegalovirus Infection

2016 ◽  
Vol 7 ◽  
Author(s):  
Maja Arapović ◽  
Ilija Brizić ◽  
Branka Popović ◽  
Slaven Jurković ◽  
Stefan Jordan ◽  
...  
Keyword(s):  
Cytomegalovirus Infection ◽  
Nk Cell ◽  
Mouse Cytomegalovirus ◽  
Cell Homeostasis

scholarly journals Cutting Edge: IL-15-Independent NK Cell Response to Mouse Cytomegalovirus Infection

2009 ◽  
Vol 183 (5) ◽  
pp. 2911-2914 ◽  
Author(s):  
Joseph C. Sun ◽  
Averil Ma ◽  
Lewis L. Lanier
Keyword(s):  
Cell Response ◽  
Cytomegalovirus Infection ◽  
Nk Cell ◽  
Cutting Edge ◽  
Mouse Cytomegalovirus

The specific NK cell response in concert with perforin prevents CD8+ T cell-mediated immunopathology after mouse cytomegalovirus infection

2015 ◽  
Vol 204 (3) ◽  
pp. 335-344 ◽  
Author(s):  
Jurica Arapović ◽  
Maja Arapović ◽  
Mijo Golemac ◽  
Luka Traven ◽  
Jelena Tomac ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Response ◽  
Cytomegalovirus Infection ◽  
Nk Cell ◽  
Cd8 T Cell ◽  
Mouse Cytomegalovirus

scholarly journals EBI3 regulates the NK cell response to mouse cytomegalovirus infection

2017 ◽  
Vol 114 (7) ◽  
pp. 1625-1630 ◽  
Author(s):  
Helle Jensen ◽  
Shih-Yu Chen ◽  
Lasse Folkersen ◽  
Garry P. Nolan ◽  
Lewis L. Lanier
Keyword(s):  
Nk Cells ◽  
Cytomegalovirus Infection ◽  
Nk Cell ◽  
Serum Levels ◽  
Dendritic Cell Maturation ◽  
Mouse Cytomegalovirus ◽  
Mcmv Infection ◽  
Barr Virus ◽  
Cd69 Expression ◽  
Epstein Barr

Natural killer (NK) cells are key mediators in the control of cytomegalovirus infection. Here, we show that Epstein–Barr virus-induced 3 (EBI3) is expressed by human NK cells after NKG2D or IL-12 plus IL-18 stimulation and by mouse NK cells during mouse cytomegalovirus (MCMV) infection. The induction of EBI3 protein expression in mouse NK cells is a late activation event. Thus, early activation events of NK cells, such as IFNγ production and CD69 expression, were not affected in EBI3-deficient (Ebi3−/−) C57BL/6 (B6) mice during MCMV infection. Furthermore, comparable levels of early viral replication in spleen and liver were observed in MCMV-infectedEbi3−/−and wild-type (WT) B6 mice. Interestingly, the viral load in salivary glands and oral lavage was strongly decreased in the MCMV-infectedEbi3−/−B6 mice, suggesting that EBI3 plays a role in the establishment of MCMV latency. We detected a decrease in the sustained IL-10 production by NK cells and lower serum levels of IL-10 in the MCMV-infectedEbi3−/−B6 mice. Furthermore, we observed an increase in dendritic cell maturation markers and an increase in activated CD8+T cells. Thus, EBI3 dampens the immune response against MCMV infection, resulting in prolonged viral persistence.

scholarly journals The NK Cell Response to Mouse Cytomegalovirus Infection Affects the Level and Kinetics of the Early CD8+ T-Cell Response

2011 ◽  
Vol 86 (4) ◽  
pp. 2165-2175 ◽  
Author(s):  
M. Mitrovic ◽  
J. Arapovic ◽  
S. Jordan ◽  
N. Fodil-Cornu ◽  
S. Ebert ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Response ◽  
Cytomegalovirus Infection ◽  
Nk Cell ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Mouse Cytomegalovirus ◽  
Kinetics Of

scholarly journals NK cell activation through the NKG2D ligand MULT-1 is selectively prevented by the glycoprotein encoded by mouse cytomegalovirus gene m145

2005 ◽  
Vol 201 (2) ◽  
pp. 211-220 ◽  
Author(s):  
Astrid Krmpotic ◽  
Milena Hasan ◽  
Andrea Loewendorf ◽  
Tanja Saulig ◽  
Anne Halenius ◽  
...  
Keyword(s):  
Cell Activation ◽  
Nk Cell ◽  
Surface Expression ◽  
Viral Gene ◽  
Nkg2d Ligand ◽  
Mouse Cytomegalovirus ◽  
Mcmv Infection ◽  
Viral Survival ◽  
Necessary And Sufficient

The NK cell–activating receptor NKG2D interacts with three different cellular ligands, all of which are regulated by mouse cytomegalovirus (MCMV). We set out to define the viral gene product regulating murine UL16-binding protein-like transcript (MULT)-1, a newly described NKG2D ligand. We show that MCMV infection strongly induces MULT-1 gene expression, but surface expression of this glycoprotein is nevertheless completely abolished by the virus. Screening a panel of MCMV deletion mutants defined the gene m145 as the viral regulator of MULT-1. The MCMV m145-encoded glycoprotein turned out to be necessary and sufficient to regulate MULT-1 by preventing plasma membrane residence of MULT-1. The importance of MULT-1 in NK cell regulation in vivo was confirmed by the attenuating effect of the m145 deletion that was lifted after NK cell depletion. Our findings underline the significance of escaping MULT-1/NKG2D signaling for viral survival and maintenance.

Sign in / Sign up

Export Citation Format

Share Document