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Nat Commun. 2018 Aug 7;9(1):3136. doi: 10.1038/s41467-018-05519-4.

Critical role of CD4+ T cells and IFNγ signaling in antibody-mediated resistance to Zika virus infection.

Author information

1
Laboratório de Inflamação e Imunidade, Departamento de Imunologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
2
Laboratório de Bacteriologia e Imunologia Clínica, Faculdade de Farmácia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
3
Laboratório de Genética de Imunologia de Infecções Virais, Departamento de Virologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
4
Laboratório de Sinalização e Imunoreceptores, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
5
Laboratório de Alvos Moleculares, Departamento de Biotecnologia Farmacêutica, Faculdade de Farmácia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
6
Department of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, 06519, USA.
7
Laboratório de Imunologia Molecular, Departamento de Imunologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
8
Laboratório de Neurobiologia Celular e Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil.
9
Laboratório de Inflamação e Imunidade, Departamento de Imunologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, 21941-902, Brazil. mbozza@micro.ufrj.br.

Abstract

Protective adaptive immunity to Zika virus (ZIKV) has been mainly attributed to cytotoxic CD8+ T cells and neutralizing antibodies, while the participation of CD4+ T cells in resistance has remained largely uncharacterized. Here, we show a neutralizing antibody response, dependent on CD4+ T cells and IFNγ signaling, which we detected during the first week of infection and is associated with reduced viral load in the brain, prevention of rapid disease onset and survival. We demonstrate participation of these components in the resistance to ZIKV during primary infection and in murine adoptive transfer models of heterologous ZIKV infection in a background of IFNR deficiency. The protective effect of adoptively transferred CD4+ T cells requires IFNγ signaling, CD8+ T cells and B lymphocytes in recipient mice. Together, this indicates the importance of CD4+ T cell responses in future vaccine design for ZIKV.

PMID:
30087337
PMCID:
PMC6081430
DOI:
10.1038/s41467-018-05519-4
[Indexed for MEDLINE]
Free PMC Article

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