Napredna pretraga

Pregled bibliografske jedinice broj: 890211

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


Nabekura, T; Gotthardt, D; Niizuma, K; Tršan, Tihana; Jenuš, Tina; Jonjić, Stipan, Lanier, LL
Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection. // The Journal of Immunology, 199 (2017), 5; 1567-1571 doi:10.4049/jimmunol.1700799 (međunarodna recenzija, članak, znanstveni)


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

Autori
Nabekura, T ; Gotthardt, D ; Niizuma, K ; Tršan, Tihana ; Jenuš, Tina ; Jonjić, Stipan, Lanier, LL

Izvornik
The Journal of Immunology (0022-1767) 199 (2017), 5; 1567-1571

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

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

Sažetak
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.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti



POVEZANOST RADA


Projekt / tema
062-0621261-1263 - Molekularni mehanizmi citomegalovirusnog izmicanja imunološkom nadzoru (Stipan Jonjić, )

Ustanove
Medicinski fakultet, Rijeka

Časopis indeksira:


  • Web of Science Core Collection (WoSCC)
    • Science Citation Index Expanded (SCI-EXP)
  • Scopus
  • MEDLINE


Citati