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Systematic analysis of innate lymphoid cells and natural killer cells in context of HIV-1 infection

ABSTRACT: We performed bulk and single cell RNA-Seq and ATAC-Seq of CD56-, CD56dim, CD56hi NK cells and innate lymphoid cells, revealed relationship among these developmental related populations, investigated the effect of HIV-1 infection on these innate populations. These findings clarify the interrelatedness of ILC populations disrupted by HIV-1 infection and provide insight into how these functions might be restored.

ORGANISM(S): Homo sapiens

PROVIDER: GSE168212 | GEO | 2021/03/04

REPOSITORIES: GEO

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Clarification of human blood ILC subtype interrelatedness and discovery of amphiregulin production by human NK cells shed light on HIV-1 pathogenesis

Project description:Human blood innate lymphoid cells (ILCs), which include ILCs and natural killer (NK) cells, derive from a common CD117+ILC precursor (ILCP). Yet, the relationship among the ILC subsets remains unclear. Bulk and single cell RNA-Seq and ATAC-Seq showed that blood ILC subsets cluster into ILC2s, ILCPs, a mixed cluster of CD56dim and CD56– NK cells, and a separate cluster of CD56hiNK cells that shares features with both ILCs and CD56dim/–NK cells. In surprising contrast to mice, tissue repair protein amphiregulin (AREG) was produced by human NK cells, with even higher levels in CD56hiNK cells than in ILCs. AREG expression in NK cells was driven by TCF7/WNT signaling and inhibited by TGFB1, a cytokine elevated in HIV-1+ people. Knockout of RUNX3, a WNT antagonist acting downstream of TGFB1, increased AREG production. Consistent with these findings, AREG+NK cells were decreased in people living with HIV-1. Additionally, functionally defective CD56–NK cells expanded in HIV-1+ people, in inverse correlation with CD56dimNK cells, ILCs, and CD4+T cells. Experiments in tissue culture and in humanized mice showed that CD56–NK cells derive from the epigenetically similar CD56dimNK cells, and that stimulation of MTOR by CD4+T cells or exogenous IL-2 prevents their expansion. These findings clarify how ILC subsets are related to each other and provide insight into how HIV-1 infection disrupts ILC homeostasis and contributes to pathology

2023-06-07 | GSE203002 | GEO

Identification of pathogenic TRAIL-expressing innate immune cells during HIV-1 infection in humanized mice by scRNA-seq

Project description:We employed the single-cell RNA sequencing (scRNA-seq) technology to study HIV-induced transcriptomic change in innate immune cells in lymphoid organs. We performed scRNA-seq on hCD45+hCD3-hCD19- human leukocytes isolated from spleens of humanized NOD/Rag2-/- /γc-/- (NRG) mice transplanted with human CD34+ hematopoietic stem-progenitor cells (NRG-hu HSC mice). We identified major populations of innate immune cells including plasmacytoid dendritic cells (pDC), myeloid dendritic cells (mDC), macrophage, nature killer (NK) cells and innate lymphoid cells (ILC). HIV-1 infection significantly upregulated genes involved in type-I interferon inflammatory pathways in each of the innate immune subsets. Interestingly, we found that the TNF-related apoptosis-inducing ligand (TRAIL) was upregulated in the innate immune populations including pDC, mDC, macrophage, NK and ILC. In summary, we characterized HIV-induced transcriptomic changes of innate immune cells in the spleen at single-cell levels, identified the TRAIL+ innate immune cells and defined an important role of TRAIL signaling pathway in HIV-1 induced CD4+ T cell depletion in vivo.

2020-06-04 | GSE148796 | GEO

CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell comparison

Project description:CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell comparison

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CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin histone modification assay

Project description:CUT and RUN was performed for 3 NK populations and found CD94+CD56hi NK cells exhibit unique H3K4me1, H3K4me4 enriched region, we also identified TCF7 binding region in CD94+CD56hi NK cells.

2019-12-10 | GSE122549 | GEO

HIV-1 perturbs homeostatic ILCs, unmasks ILC1 plasticity, and boosts TCF7+ memory NK cells

Project description:Bulk RNA-seq, and single cell RNA-Seq using inDrops methodology, were used to compare two populations of cells that had been sorted by flow cytometry from human peripheral blood mononuclear cells (PBMCs) from two donors, G27 and G33. To sort the cells, PBMCs were stained with antibodies to 11 lineage markers (FITC), anti-CD56 (PE), and anti-CD94 (APC). The 11 lineage marker positive cells were excluded to identify the innate lymphocyte cell (ILC) population. Then we sorted the Lin-CD56+CD94- cells (CD127-ILC1s, 'neg') from the Lin-CD56+CD94+ cells (NK cells, 'pos') with a BD FACSAria IIu. Libraries were generated from each of these two populations.

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CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell comparison

Project description:We compared transcriptomes of 3 NK populations and found CD94+CD56hi NK cells exhibit unique transcriptome.

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CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin accessibility assay

Project description:CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin accessibility assay

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CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin accessibility assay

Project description:ATAC-Seq was performed for 3 NK populations and found CD94+CD56hi NK cells exhibit unique chromatin accessible region

2019-12-10 | GSE122548 | GEO

CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin histone modification assay

Project description:CD94-CD56dim, CD94+CD56dim and CD94+CD56hi natural killer (NK) cell chromatin histone modification assay

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RORÎ³t+ Innate lymphoid cells transcriptomes after aNKp44 and cytokine stimulation

Project description:RORÎ³t+ innate lymphoid cells (ILC) are crucial players of innate immune responses and represent a major source of IL-22, which has an important role in mucosal homeostasis. The signals required by RORÎ³t+ ILC to express IL-22 and other cytokines, including TNF, have only partially been elucidated. Here we show that RORÎ³t+ ILC can directly sense the environment by the engagement of the activating receptor NKp44. NKp44 triggering in RORÎ³t+ ILC selectively activates a coordinated pro-inflammatory program, including TNF, while cytokine stimulation induces preferentially IL-22 expression. However, combined engagement of NKp44 and cytokine receptors results in a strong synergistic effect. These data support the concept that NKp44+ RORÎ³t+ ILC can be activated without cytokines and are able to switch between IL-22 or TNF production, depending on the triggering stimulus. Transcriptome analysis of CD56+CD127hi tonsil ILC, Ex vivo and after stimulation with aNKp44, IL-1/IL-7/IL-23 or aNKp44/IL-1/IL-7/IL-23 for 3.5h. RNA was extracted and pooled from 2 donors each, Amplified and labeled according to manufacturerÂ´s instructions (GeneChipU133plus2Â® , Affymetrix). The analysis was performed in triplicates.

2013-10-30 | E-GEOD-43409 | biostudies-arrayexpress

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