Cutting Edge: NKG2D signaling enhances NK cell responses but alone is insufficient to drive expansion during mouse Cytomegalovirus infection (CROSBI ID 241881)
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Podaci o odgovornosti
Nabekura, T ; Gotthardt, D ; Niizuma, K ; Tršan, Tihana ; Jenuš, Tina ; Jonjić, Stipan ; Lanier, Lewis L.
engleski
Cutting Edge: NKG2D signaling enhances NK cell responses but alone is insufficient to drive expansion during mouse Cytomegalovirus infection
NK cells play a critical role in host defense against viruses. In this study, we investigated the role of NKG2D in the expansion of NK cells after mouse CMV (MCMV) infection. Wild-type and NKG2D-deficient (Klrk12/2) Ly49H+ NK cells proliferated robustly when infected with MCMV strains engineered to allow expression of NKG2D ligands, which enhanced the response of wild-type NK cells. Naive NK cells exclusively express NKG2D-L, which pairs only with DAP10, whereas NKG2D-S expressed by activated NK cells pairs with DAP10 and DAP12, similar to Ly49H. However, NKG2D alone was unable to drive robust expansion of Ly49H2 NK cells when mice were infected with these MCMV strains, likely because NKG2D-S was only transiently expressed postinfection. These findings demonstrate that NKG2D augments Ly49H-dependent proliferation of NK cells ; however, NKG2D signaling alone is inadequate for expansion of NK cells, likely due to only transient expression of the NKG2D–DAP12 complex.
NKG2D signaling ; NK cell ; response ; mouse ; Cytomegalovirus infection
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Podaci o izdanju
199 (5)
2017.
1567-1571
objavljeno
0022-1767
1550-6606
10.4049/jimmunol.1700799
Povezanost rada
Temeljne medicinske znanosti