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HIV specific CD8+ Trm-like cells in tonsils express exhaustive signatures in the absence of natural HIV control [smart-seq 2]

ABSTRACT: HIV specific CD8+ Trm-like cells in tonsils express exhaustive signatures in the absence of natural HIV control [smart-seq 2]

PROVIDER: PRJNA888963 | ENA |

REPOSITORIES: ENA

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HIV specific CD8+ Trm-like cells in tonsils express exhaustive signatures in the absence of natural HIV control [smart-seq 2]

Project description:Lymphoid tissues are an important HIV reservoir site that persists in the face of antiretroviral therapy and natural immunity. Targeting these reservoirs by harnessing the antiviral activity of local tissue-resident memory (TRM) CD8+ T-cells is of great interest, but limited data exist on TRM-like cells within lymph nodes of people living with HIV (PLWH). Here, we studied tonsil CD8+ T-cells obtained from PLWH and uninfected controls from South Africa. We show that these cells are preferentially located outside the germinal centers (GCs), the main reservoir site for HIV, and display a low cytolytic and transcriptionally TRMlike profile distinct from blood CD8+ T-cells. In PLWH, CD8+ TRM-like cells are highly expanded and adopt a more cytolytic, activated, and exhausted phenotype not reversed by antiretroviral therapy (ART). This phenotype was enhanced in HIV-specific CD8+ T-cells from tonsils compared to matched blood suggesting a higher antigen burden in tonsils. Single-cell transcriptional and clonotype resolution showed that these HIV-specific CD8+ T-cells in the tonsils express heterogeneous signatures of T-cell activation, clonal expansion, and exhaustion ex-vivo. Interestingly, this signature was absent in a natural HIV controller, who expressed lower PD-1 and CXCR5 levels and reduced transcriptional evidence of T-cell activation, exhaustion, and cytolytic activity. These data provide important insights into lymphoid tissue-derived HIVspecific CD8+ TRM-like phenotypes in settings of HIV remission and highlight their potential for immunotherapy and targeting of the HIV reservoirs.

2022-10-12 | GSE215126 | GEO

HIV specific CD8+ Trm-like cells in tonsils express exhaustive signatures in the absence of natural HIV control [Seqwell]

2022-10-12 | GSE215125 | GEO

HIV specific CD8+ Trm-like cells in tonsils express exhaustive signatures in the absence of natural HIV control

Project description:HIV specific CD8+ Trm-like cells in tonsils express exhaustive signatures in the absence of natural HIV control

| PRJNA888959 | ENA

HIV specific CD8+ Trm-like cells in tonsils express exhaustive signatures in the absence of natural HIV control [Seqwell]

Project description:HIV specific CD8+ Trm-like cells in tonsils express exhaustive signatures in the absence of natural HIV control [Seqwell]

| PRJNA888964 | ENA

HIV specific CD8+ Trm-like cells in tonsils express exhaustive signatures in the absence of natural HIV control

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

2022-10-12 | GSE215127 | GEO

Smart RNA sequencing Facilitates Quantitative Analysis of dermal CD4+ Trm cells between SLE and NC.

Project description:The goals of this study are to compare transcriptome of dermis-derived CD4+ Trm cells between SLE and NC.

2024-08-06 | GSE181613 | GEO

TNF dependent induction of inhibitory pathways in CD4+ T cells in HIV and LCMV [HIV-infected individuals]

Project description:Chronic viral infections caused by HIV in humans or LCMV in mice are characterized by immunodeficiency and chronic inflammation. During chronification, T cells progressively lose effector functions, a process associated with immunoregulatory pathways and known as T-cell exhaustion. A link between ‘exhaustive’ T-cell reprogramming and chronic inflammation has not been established. Using a systems biology approach we demonstrate in HIV and LCMV infection that TNF, a prototypical mediator of chronic inflammation, functions upstream of major immunoregulatory pathways in T cells during chronic viral infection. In vivo blockade of TNFR-signaling interferes with the exhaustive T-cell program during chronic infection and reduces viral loads by several log. Continuous TNFR-signaling during disease progression towards chronic infection seems to be causative for T-cell exhaustion and an important link between immunodeficiency and chronic inflammation. TNF blockade might represent a novel therapeutic option during late stage infections caused by HIV and other virus causing chronic infections.

2016-03-07 | GSE17606 | GEO

Campylobacter-infected chicken caecal tonsils

Project description:Campylobacter-infected chicken caecal tonsils

| PRJEB22580 | ENA

TNF dependent induction of inhibitory pathways in CD4+ T cells in HIV and LCMV [CD4+ T activation]

2016-03-07 | GSE17946 | GEO

Hobit identifies TRM precursors that are regulated by Eomes

Project description:Tissue-resident memory CD8+ T cells (TRM) constitute a non-circulating memory T cell subset that provides early protection against re-infection. However, how TRM arise from antigen-triggered T cells has remained unclear. Exploiting the TRM-restricted expression of Hobit, we developed TRM reporter/deleter mice to study TRM differentiation. We found that Hobit was upregulated in a subset of LCMV-specific T cells located within peripheral tissues during the effector phase of the immune response. These Hobit+ effector T cells were identified as TRM precursors, given that their depletion substantially decreased TRM development, but not the formation of circulating memory T cells. Adoptive transfer experiments of Hobit+ effector T cells corroborated their biased contribution to the TRM lineage. Transcriptional profiling of Hobit+ effector T cells underlined the early establishment of TRM properties including downregulation of tissue exit receptors and upregulation of TRM-associated molecules. Importantly, we identified Eomes as a key factor instructing the early bifurcation of circulating and resident lineages. These findings establish that commitment of TRM occurs early in antigen-driven T cell differentiation and reveal the molecular mechanisms underlying this differentiation pathway.

2021-08-19 | GSE182343 | GEO

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