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Tissue-Specific Determinants of Adaptive NK Cell Responses - Myeloid Cells

ABSTRACT: Tissue-Specific Determinants of Adaptive NK Cell Responses - Myeloid Cells

PROVIDER: PRJNA975928 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24727200_1.fastq.gz	Fastqsanger.gz
	SRR24727200_2.fastq.gz	Fastqsanger.gz
	SRR24727201_1.fastq.gz	Fastqsanger.gz
	SRR24727201_2.fastq.gz	Fastqsanger.gz
	SRR24727202_1.fastq.gz	Fastqsanger.gz

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Tissue-Specific Determinants of Adaptive NK Cell Responses

Project description:Tissue-Specific Determinants of Adaptive NK Cell Responses

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Tissue-Specific Determinants of Adaptive NK Cell Responses - Myeloid Cells

Project description:Natural killer (NK) cells are circulating lymphocytes that possess both innate and adaptive features, the latter including antigen-specific clonal expansion and long-lived memory responses. Unlike other adaptive lymphocytes like T and B cells, NK cells are not thought to require priming in lymphoid organs during activation. However, although NK cells respond in multiple tissue sites during cytomegalovirus (CMV) infection, here we observed that early activation and virus-specific expansion occurs predominantly in the spleen. These splenic NK cells exhibited heightened TNF-a signaling, which we identify as a novel and critical regulator of both innate and adaptive responses through engagement of distinct NF-kB signaling arms downstream of TNFR2. These findings highlight the central role of the spleen as a lymphoid organ in facilitating the innate-to-adaptive transition NK cells undergo during viral infection, and provide insight into how we can better generate innate and adaptive NK cell immunity across diverse settings. Bulk RNA-Seq data of cDC1, pDC, red pulp macrophages from spleen at different time points post MCMV infection

2025-02-28 | GSE233346 | GEO

Tissue-Specific Determinants of Adaptive NK Cell Responses - WT vs TNFR2ko NK

Project description:Tissue-Specific Determinants of Adaptive NK Cell Responses - WT vs TNFR2ko NK

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Tissue-Specific Determinants of Adaptive NK Cell Responses - Spleen vs Liver NK

Project description:Tissue-Specific Determinants of Adaptive NK Cell Responses - Spleen vs Liver NK

| PRJNA975930 | ENA

Tissue-Specific Determinants of Adaptive NK Cell Responses - Spleen vs Liver NK

Project description:Natural killer (NK) cells are circulating lymphocytes that possess both innate and adaptive features, the latter including antigen-specific clonal expansion and long-lived memory responses. Unlike other adaptive lymphocytes like T and B cells, NK cells are not thought to require priming in lymphoid organs during activation. However, although NK cells respond in multiple tissue sites during cytomegalovirus (CMV) infection, here we observed that early activation and virus-specific expansion occurs predominantly in the spleen. These splenic NK cells exhibited heightened TNF-a signaling, which we identify as a novel and critical regulator of both innate and adaptive responses through engagement of distinct NF-kB signaling arms downstream of TNFR2. These findings highlight the central role of the spleen as a lymphoid organ in facilitating the innate-to-adaptive transition NK cells undergo during viral infection, and provide insight into how we can better generate innate and adaptive NK cell immunity across diverse settings. Bulk RNA-Seq data of WT Ly49H+ NK from spleen or liver on day 0 and day 1 post MCMV infection.

2025-02-28 | GSE233347 | GEO

Tissue-Specific Determinants of Adaptive NK Cell Responses - WT vs TNFR2ko NK

Project description:Natural killer (NK) cells are circulating lymphocytes that possess both innate and adaptive features, the latter including antigen-specific clonal expansion and long-lived memory responses. Unlike other adaptive lymphocytes like T and B cells, NK cells are not thought to require priming in lymphoid organs during activation. However, although NK cells respond in multiple tissue sites during cytomegalovirus (CMV) infection, here we observed that early activation and virus-specific expansion occurs predominantly in the spleen. These splenic NK cells exhibited heightened TNF-a signaling, which we identify as a novel and critical regulator of both innate and adaptive responses through engagement of distinct NF-kB signaling arms downstream of TNFR2. These findings highlight the central role of the spleen as a lymphoid organ in facilitating the innate-to-adaptive transition NK cells undergo during viral infection, and provide insight into how we can better generate innate and adaptive NK cell immunity across diverse settings. Bulk RNA-Seq data of WT or TNFR2-/- Ly49H+ NK from spleen at different time points post MCMV infection.

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Expression analysis of canonical and adaptive human NK cell subsets

Project description:The mechanisms underlying human natural killer (NK) cell phenotypic and functional heterogeneity are unknown. Here, we have described the emergence of diverse subsets of human NK cells selectively lacking expression of signaling proteins following cytomegalovirus (CMV) infection. The absence of B and myeloid cell-related signaling protein expression in these NK cell subsets correlated with promoter DNA hypermethylation. Genome-wide DNA methylation patterns were strikingly similar between CMV-associated adaptive NK cells and cytotoxic effector T cells, but differed from those of canonical NK cells. Functional interrogation demonstrated altered cytokine responsiveness in adaptive NK cells that was linked to reduced expression of the transcription factor PLZF. Furthermore, subsets of adaptive NK cells demonstrated significantly reduced functional responses to activated autologous T cells. The present results uncover a spectrum of epigenetically unique adaptive NK cell subsets that diversify in response to viral infection and have distinct functional capabilities compared to canonical NK cell subsets.

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CMV infection drives adaptive epigenetic diversification of NK cells

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2015-03-06 | E-GEOD-66562 | biostudies-arrayexpress

Transcriptional and epigenetic regulation of adaptive NK cell responses [ChIP-Seq]

Project description:Transcriptional and epigenetic regulation of adaptive NK cell responses [ChIP-Seq]

| PRJNA415720 | ENA