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ILC1 confer early host protection at initial sites of viral infection

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE103904 | GEO | 2017/11/01

SECONDARY ACCESSION(S): PRJNA407437

REPOSITORIES: GEO

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ILC1 Confer Early Host Protection at Initial Sites of Viral Infection.

Project description:Infection is restrained by the concerted activation of tissue-resident and circulating immune cells. Whether tissue-resident lymphocytes confer early antiviral immunity at local sites of primary infection prior to the initiation of circulating responses is not well understood. Furthermore, the kinetics of initial antiviral responses at sites of infection remain unclear. Here, we show that tissue-resident type 1 innate lymphoid cells (ILC1) serve an essential early role in host immunity through rapid production of interferon (IFN)-γ following viral infection. Ablation of Zfp683-dependent liver ILC1 lead to increased viral load in the presence of intact adaptive and innate immune cells critical for mouse cytomegalovirus (MCMV) clearance. Swift production of interleukin (IL)-12 by tissue-resident XCR1+ conventional dendritic cells (cDC1) promoted ILC1 production of IFN-γ in a STAT4-dependent manner to limit early viral burden. Thus, ILC1 contribute an essential role in viral immunosurveillance at sites of initial infection in response to local cDC1-derived proinflammatory cytokines.

| S-EPMC5687850 | biostudies-literature

ILC1 confer early host protection at initial sites of viral infection [RNA-Seq]

Project description:We show that tissue-resident ILC1 serve a non-redundant early role in host immunity through rapid production of interferon (IFN)-γ following mouse cytomegalovirus (MCMV) infection.

2017-11-01 | GSE103901 | GEO

ILC1 confer early host protection at initial sites of viral infection [ATAC-Seq]

2017-11-01 | GSE103900 | GEO

ILC1 confer early host protection at initial sites of viral infection

Project description:ILC1 confer early host protection at initial sites of viral infection

| PRJNA407437 | ENA

Gut microbiota-derived metabolites confer protection against SARS-CoV-2 infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-08-02 | GSE189794 | GEO

Monocyte-derived alveolar macrophages induced by influenza infection confer long-term antibacterial protection

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-01-13 | GSE120543 | GEO

Epigenetic reprogramming of host and viral genes by Human Cytomegalovirus infection in Kasumi-3 myeloid progenitor cells at early times post-infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-03-05 | GSE164861 | GEO

Gut microbiota-derived metabolites confer protection against SARS-CoV-2 infection.

Project description:The gut microbiome is intricately coupled with immune regulation and metabolism, but its role in Coronavirus Disease 2019 (COVID-19) is not fully understood. Severe and fatal COVID-19 is characterized by poor anti-viral immunity and hypercoagulation, particularly in males. Here, we define multiple pathways by which the gut microbiome protects mammalian hosts from SARS-CoV-2 intranasal infection, both locally and systemically, via production of short-chain fatty acids (SCFAs). SCFAs reduced viral burdens in the airways and intestines by downregulating the SARS-CoV-2 entry receptor, angiotensin-converting enzyme 2 (ACE2), and enhancing adaptive immunity via GPR41 and 43 in male animals. We further identify a novel role for the gut microbiome in regulating systemic coagulation response by limiting megakaryocyte proliferation and platelet turnover via the Sh2b3-Mpl axis. Taken together, our findings have unraveled novel functions of SCFAs and fiber-fermenting gut bacteria to dampen viral entry and hypercoagulation and promote adaptive antiviral immunity.

| S-EPMC9348133 | biostudies-literature

Diagnosis of childhood bacterial and viral infection using host RNA expression

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-08-29 | GSE72829 | GEO

Human NK cells confer protection against HIV-1 infection in humanized mice.

Project description:The role of NK cells against HIV-1 infections remains to be elucidated in vivo. While humanized mouse models potentially could be used to directly evaluate human NK cell responses during HIV-1 infection, improved functional development of human NK cells in these hosts is needed. Here, we report the humanized MISTRG-6-15 mouse model, in which NK cells were quick to expand and exhibit degranulation, cytotoxicity, and proinflammatory cytokine production in nonlymphoid organs upon HIV-1 infection but had reduced functionality in lymphoid organs. Although HIV-1 infection induced functional impairment of NK cells, antiretroviral therapy reinvigorated NK cells in response to HIV-1 rebound after analytic treatment interruption. Moreover, a broadly neutralizing antibody, PGT121, enhanced NK cell function in vivo, consistent with antibody-dependent cellular cytotoxicity. Monoclonal antibody depletion of NK cells resulted in higher viral loads in multiple nonlymphoid organs. Overall, our results in humanized MISTRG-6-15 mice demonstrated that NK cells provided direct anti-HIV-1 responses in vivo but were limited in their responses in lymphoid organs.

| S-EPMC9753998 | biostudies-literature

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