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Human inflammatory mucosal T cells in the female reproductive tract are poised to participate in immunity to infection

ABSTRACT: Human inflammatory mucosal T cells in the female reproductive tract are poised to participate in immunity to infection

PROVIDER: PRJNA525619 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8668830.fastq.gz	Fastqsanger.gz
	SRR8668840.fastq.gz	Fastqsanger.gz
	SRR8668850.fastq.gz	Fastqsanger.gz
	SRR8668860.fastq.gz	Fastqsanger.gz
	SRR8668870.fastq.gz	Fastqsanger.gz

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Human inflammatory mucosal T cells in the female reproductive tract are poised to participate in immunity to infection

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Seminal plasma exposures strengthen vaccine responses in the female reproductive tract mucosae

Project description:HIV-1 sexual transmission occurs mainly via mucosal semen exposures. In the female reproductive tract (FRT), seminal plasma (SP) induces physiological modifications, including inflammation. An effective HIV-1 vaccine should elicit mucosal immunity. However, modifications of vaccine responses by the local environment remain to be characterized. Using a modified vaccinia virus Ankara (MVA) as a vaccine model, we characterized the impact of HIV-1+ SP intravaginal exposure on the local immune responses of nonhuman primates. Multiple HIV-1+ SP exposures did not impact the anti-MVA antibody responses. However, SP exposures revealed an anti-MVA responses mediated by CD4+ T cells, which was not observed in the control group. Multi-parameter approaches clearly identified the cervix as the most impacted compartment in the FRT. The frequency and the quality of specific anti-MVA CD8+ T cell responses increased in the FRT exposed to SP. Furthermore SP exposures induced a local cell recruitment of antigen presenting cells, especially CD11c+ cells and CD8+ T cell recruitment in the FRT draining lymph nodes. CD11c+ cell recruitment was associated with upregulation of inflammation-related gene expression after SP exposures in the cervix. We thus highlight the fact that physiological conditions, such as SP exposures, should be taken into consideration to test and to improve vaccine efficacy against HIV-1 and other sexually transmitted infections.

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Project description:Interferon ε (IFNε), a unique type I IFN, is thought to protect the host against sexually transmitted infections. Unlike conventional type I IFNs (e.g., IFNα/β), whose expression is undetectable at baseline, IFNε expression is detectable in the epithelium of mucosal tissues, particularly the female reproductive tract (FRT). We found that IFNε expression was not limited to epithelial cells at the FRT. Importantly, in contrast to previous reports, IFNε expression in plasmacytoid dendritic cells and primary cervical epithelial cells was induced by viral infection and by activation of TLR3 or 4 in PBMCs. Induction of IFNε mRNAs was also found in cervicovaginal tissues (CVT) of Zika virus (ZIKV)-infected mice. Mice with IFNε deficiency (Ifnε-/-) did not have impaired induction of interferon-stimulated genes except IFNl, but had altered epithelial and collagen structure in the CVT. Ifnε-/- mice exhibited increased susceptibility to ZIKV infection via an intravaginal route but not via a subcutaneous route, indicating that the protective effect of IFNe was specific to the FRT. Infected Ifnε-/- mice had higher and more sustained viral loads than infected wild-type (WT) mice. Detection of ZIKV infection by single molecule in situ hybridization confirmed that virus spread faster in Ifnε-/- mice than in WT mice. Recombinant murine IFNε protected Ifnar1-/- mice against ZIKV infection when administered through an intravaginal route but not when administered through a subcutaneous route, indicating that the specific role of IFNe at the FRT is independent of IFNAR1 signaling. Our findings indicate that IFNε mediates a novel FRT-specific protective effect on mucosal immunity that limits Zika virus spread.

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Modified Vaccinia virus Ankara vector induces specific cellular and humoral responses in the female reproductive tract, the main HIV portal of entry

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