Article
NK Cell Responses in Zika Virus Infection Are Biased towards Cytokine-Mediated Effector Functions
Registro en:
MAUCOURANT, Christopher et al. NK Cell Responses in Zika Virus Infection Are Biased towards Cytokine-Mediated Effector Functions. Journal of Immunology, v. 207, p. 1333 1343, 2021.
0022-1767
10.4049/jimmunol.2001180
Autor
Maucourant, Christopher
Queiroz, Gabriel Andrade Nonato
Corneau, Aurelien
Gois, Luana Leandro
Kheddar, Aida Meghraoui
Tarantino, Nadine
Bandeira, Antonio Carlos
Samri, Assia
Blanc, Catherine
Yssel, Hans
Grassi, Maria Fernanda Rios
Vieillard, Vincent
Resumen
European Union Horizon 2020 ZIKAlliance
Program (grant agreement 734548) and by the Coordination of Superior Level Staff
Improvement-Brazil (CAPES Finance Code 001). C.M. received a Ph.D. fellowship
from the French Ministry of Education; L.L.G. received a grant from the French Society
for Cytometry; and M.F.R.G. is a research fellow of the National Council for Scientific
and Technological Development (CNPq) and Foundation for the Development of
Private Higher Education from Brazil. Zika virus (ZIKV) is a mosquito-borne flavivirus that has emerged as a global concern because of its impact on human health.
ZIKV infection during pregnancy can cause microcephaly and other severe brain defects in the developing fetus and there have
been reports of the occurrence of Guillain-Barr e syndrome in areas affected by ZIKV. NK cells are activated during acute viral
infections and their activity contributes to a first line of defense because of their ability to rapidly recognize and kill virus-infected
cells. To provide insight into NK cell function during ZIKV infection, we have profiled, using mass cytometry, the NK cell
receptor-ligand repertoire in a cohort of acute ZIKV-infected female patients. Freshly isolated NK cells from these patients
contained distinct, activated, and terminally differentiated, subsets expressing higher levels of CD57, NKG2C, and KIR3DL1 as
compared with those from healthy donors. Moreover, KIR3DL1+ NK cells from these patients produced high levels of IFN-g and
TNF-a, in the absence of direct cytotoxicity, in response to in vitro stimulation with autologous, ZIKV-infected, monocyte-derived
dendritic cells. In ZIKV-infected patients, overproduction of IFN-g correlated with STAT-5 activation (r 5 0.6643; p 5 0.0085)
and was mediated following the recognition of MHC class 1 related chain A and chain B molecules expressed by ZIKV-infected
monocyte-derived dendritic cells, in synergy with IL-12 production by the latter cells. Together, these findings suggest that NK
cells contribute to the generation of an efficacious adaptive anti-ZIKV immune response that could potentially affect the outcome
of the disease and/or the development of persistent symptoms.
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