Genetic labeling reveals altered turnover and stability of innate lymphocytes in latent mouse cytomegalovirus infection
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Genetic labeling reveals altered turnover and stability of innate lymphocytes in latent mouse cytomegalovirus infection. / Busche, Andreas; Schmitz, Susanne; Fleige, Henrike; Robbins, Scott H; Walzer, Thierry; Stewart, Charles A; Förster, Reinhold; Messerle, Martin; Prinz, Immo.
in: J IMMUNOL, Jahrgang 186, Nr. 5, 01.03.2011, S. 2918-25.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Genetic labeling reveals altered turnover and stability of innate lymphocytes in latent mouse cytomegalovirus infection
AU - Busche, Andreas
AU - Schmitz, Susanne
AU - Fleige, Henrike
AU - Robbins, Scott H
AU - Walzer, Thierry
AU - Stewart, Charles A
AU - Förster, Reinhold
AU - Messerle, Martin
AU - Prinz, Immo
PY - 2011/3/1
Y1 - 2011/3/1
N2 - Mouse CMV (MCMV) infection rapidly induces the proliferation of NK cells, which correlates with immunological protection. Whether NK cells primed during acute response against MCMV are maintained for the long term is not known. In this study, we used TcrdH2BeGFP mice in which maturing NK cells are genetically labeled with a pulse of very stable histone-2B-eGFP. In this system, we found that the reporter protein was diluted out upon NK cell division during acute MCMV infection. At the same time, mature NK cells in uninfected mice showed only very limited turnover in vivo. Three months after primary infection when MCMV latency was established, the majority of peripheral NK cells still displayed a higher record of proliferation than NK cells in mock-infected controls. This observation included both Ly49H(+) and Ly49H(-) NK cells. Conversely, naive NK cells did not show more proliferation after transfer into latently MCMV-infected mice than that after transfer into mock-infected control mice. This indicated that the observed alterations of the NK cell compartment in MCMV latency were "legacy" (i.e., resulting from prior events during the initial immune response). Together, these results suggest that antiviral immune responses induce sustained alterations of innate lymphocyte populations that extend far beyond the first days of acute infection.
AB - Mouse CMV (MCMV) infection rapidly induces the proliferation of NK cells, which correlates with immunological protection. Whether NK cells primed during acute response against MCMV are maintained for the long term is not known. In this study, we used TcrdH2BeGFP mice in which maturing NK cells are genetically labeled with a pulse of very stable histone-2B-eGFP. In this system, we found that the reporter protein was diluted out upon NK cell division during acute MCMV infection. At the same time, mature NK cells in uninfected mice showed only very limited turnover in vivo. Three months after primary infection when MCMV latency was established, the majority of peripheral NK cells still displayed a higher record of proliferation than NK cells in mock-infected controls. This observation included both Ly49H(+) and Ly49H(-) NK cells. Conversely, naive NK cells did not show more proliferation after transfer into latently MCMV-infected mice than that after transfer into mock-infected control mice. This indicated that the observed alterations of the NK cell compartment in MCMV latency were "legacy" (i.e., resulting from prior events during the initial immune response). Together, these results suggest that antiviral immune responses induce sustained alterations of innate lymphocyte populations that extend far beyond the first days of acute infection.
KW - Acute Disease
KW - Animals
KW - Cytomegalovirus Infections/immunology
KW - Green Fluorescent Proteins/genetics
KW - Histones/genetics
KW - Immunity, Innate/genetics
KW - Killer Cells, Natural/immunology
KW - Mice
KW - Mice, Inbred C57BL
KW - Mice, Transgenic
KW - Muromegalovirus/genetics
KW - NK Cell Lectin-Like Receptor Subfamily A/biosynthesis
KW - Virus Latency/genetics
U2 - 10.4049/jimmunol.1003232
DO - 10.4049/jimmunol.1003232
M3 - SCORING: Journal article
C2 - 21270406
VL - 186
SP - 2918
EP - 2925
JO - J IMMUNOL
JF - J IMMUNOL
SN - 0022-1767
IS - 5
ER -