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The CD27/CD70 pathway negatively regulates visceral adipose tissue resident Th2 cells and controls metabolic homeostasis

ABSTRACT: The CD27/CD70 pathway negatively regulates visceral adipose tissue resident Th2 cells and controls metabolic homeostasis

PROVIDER: PRJNA1063686 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27498836_1.fastq.gz	Fastqsanger.gz
	SRR27498836_2.fastq.gz	Fastqsanger.gz
	SRR27498837_1.fastq.gz	Fastqsanger.gz
	SRR27498837_2.fastq.gz	Fastqsanger.gz
	SRR27498838_1.fastq.gz	Fastqsanger.gz

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The CD27/CD70 pathway negatively regulates visceral adipose tissue resident Th2 cells and controls metabolic homeostasis

Project description:The adipose tissue homeostasis relies on the interplay between several regulatory lineages, such as ILC2, Th2, Treg, eosinophils and type 2 macrophages. Among them, ILC2 are numerically the dominant source of type 2 cytokines and are considered as major regulators of adiposity. Despite the overlap in immune effector molecules and sensitivity to alarmins (TSLP, IL-33) between ILC2 and resident memory Th2 lymphocytes, the role of the adaptive axis of type-2 immunity remains unclear. We show that mice deficient for CD27, a member of the TNF receptor superfamily, are more resistant to obesity and associated disorders. A comparative analysis of the CD4 compartment of both strains revealed higher numbers of fat resident memory Th2 cells in the adipose tissue of CD27KO mice, which correlated with decreased PD-1-induced apoptosis. Our data point to a non-redundant role for Th2 lymphocytes in obesogenic conditions.

2024-01-31 | GSE253037 | GEO

RNA sequencing analysis of ex vivo expanded CD27+CD70- and CD27-CD70+ human regulatory T cells

Project description:Our study shows that after extended stimulation of human CD4+CD25+CD127- Tregs in vitro, a stable cell subset that downregulates CD27 and upregulates CD70 develops. Expanded CD27+CD70- Tregs display a gene profile which closely relates to the previously described “Treg gene signature”, whereas CD27-CD70+ Tregs express some genes associated with Treg gene signature and some genes overexpressed in conventional T cells.

2020-07-10 | GSE129251 | GEO

RNA sequencing analysis of ex vivo expanded CD27+CD70- and CD27-CD70+ human regulatory T cells

Project description:RNA sequencing analysis of ex vivo expanded CD27+CD70- and CD27-CD70+ human regulatory T cells

| PRJNA530612 | ENA

Transcription profiling by array of mouse wild type or CD27-/- OT-I T cells are stimulated with artficial antigen presenting cell lines expressing CD70 and/or CD80

Project description:WT or CD27-/- OT-I T cells are stimulated in vitro with artficial antigen presenting cell (aAPC) lines expressing CD70 and/or CD80 for 2, 4, 8 or 14 hours.

2010-09-29 | E-NCMF-38 | biostudies-arrayexpress

Analysis of CD70 wild type or CD70 knock out CD70-specific nanoCAR T cells

Project description:CD70 is an attractive target for chimeric antigen receptor (CAR) T cell therapy as treatment for both solid and liquid malignancies. However, functionality of CD70-specific CAR T cells is only modest. Here, we optimized a CD70-specific VHH based CAR (nanoCAR). We evaluated the nanoCARs in clinically relevant models in vitro, using co-cultures of CD70-specific nanoCAR T cells with malignant rhabdoid tumor organoids, and in vivo by using a diffuse large B cell lymphoma (DLBCL) patient-derived xenograft (PDX) model. Whereas the nanoCAR T cells were highly efficient in organoid co-cultures, they showed only modest efficacy in the PDX model. Knocking out CD70 expression in the nanoCAR T cells resulted in dramatically enhanced functionality in the PDX model, suggesting that CD70 interaction in cis with the nanoCAR induces exhaustion. Through single-cell transcriptomics, we obtained evidence that CD70 KO CD70-specific nanoCAR T cells are protected from antigen-induced exhaustion. Our data show that CARs targeted to endogenous T cell antigens, negatively affect CAR T cell functionality by inducing an exhausted state, which can be overcome by knocking out the specific target, in this case CD70.

2024-06-17 | GSE227435 | GEO

Chronic CD27-CD70 costimulation promotes type 1-specific polarization of effector Tregs

Project description:Chronic CD27-CD70 costimulation promotes type 1-specific polarization of effector Tregs

| PRJNA885122 | ENA

Analysis of CD70 wild type or CD70 knock out CD70-specific nanoCAR T cells [RNA-Seq]

Project description:CD70 is an attractive target for chimeric antigen receptor (CAR) T-cell therapy for the treatment of both solid and liquid malignancies. However, the functionality of CD70-specific CAR T-cells is modest. We optimized a CD70-specific VHH-based CAR (nanoCAR). We evaluated the nanoCARs in clinically relevant models in vitro, using co-cultures of CD70-specific nanoCAR T-cells with malignant rhabdoid tumor organoids, and in vivo using a diffuse large B-cell lymphoma (DLBCL) patient-derived xenograft (PDX) model. Whereas the nanoCAR T-cells were highly efficient in organoid co-cultures, they showed only modest efficacy in the PDX model. Fratricide was not causing this loss in efficacy but rather CD70 interaction in cis with the nanoCAR, as validated by imaging flowcytometry, induces exhaustion. Knocking out CD70 expression in nanoCAR T-cells using CRISPR/Cas9, resulted in dramatically enhanced functionality in the DLBCL PDX model. Through single-cell transcriptomics, we obtained evidence that CD70 knock out (KO) CD70-specific nanoCAR T-cells were protected from antigen-induced exhaustion. In addition, we were able to demonstrate that WT CD70-specific nanoCAR T-cells already exhibit signs of exhaustion shortly after production. Their gene signature strongly overlapped with gene signatures of exhausted CAR T-cells. On the other hand, the gene signature of KO nanoCAR T-cells overlapped with the gene signature of CAR T-cell infusion products that led to complete responses in chronic lymphatic leukemia patients. Our data show that CARs targeting endogenous T-cell antigens, negatively affect CAR T-cell functionality by inducing an exhausted state, which can be overcome by knocking out the specific target, in this case CD70.

2024-06-17 | GSE265937 | GEO

Chronic CD27-CD70 costimulation promotes type 1-specific polarization of effector Tregs

Project description:Most T lymphocytes, including regulatory T cells, express the CD27 costimulatory receptor in steady state conditions. There is evidence that CD27 engagement on conventional T lymphocytes favors the development of Th1 and cytotoxic responses in mice and humans, but the impact on the regulatory lineage is unknown. In this report, we examined the effect of constitutive CD27 engagement on both regulatory and conventional CD4+ T cells in vivo, in the absence of intentional antigenic stimulation. Our data show that both T cell subsets convert into type 1 effectors, characterized by cell activation, cytokine production, response to IFN-and CXCR3-dependent migration to inflammatory sites. Our data highlight the role of the transcription factor Eomes in this process. We conclude that CD27 may regulate the development of Th1 immunity in peripheral tissues as well as the subsequent switch of the effector response into long-term memory.

2022-11-30 | GSE214395 | GEO

Autosomal Recessive CD70 Deficiency

Project description:<p>We describe four patients from two unrelated families of different ethnicities who had primary immunodeficiency predominantly manifesting as susceptibility to EBV-related diseases. We performed whole exome sequencing (P1 and P2 from family 1) or whole genome sequencing (P4 and both parents from family 2) in those two families and identified homozygous frameshift or in-frame deletions in CD70 in these patients which abolished either CD70 surface expression or binding to its counter structure CD27. Sanger sequencing identified the same homozygous <i>CD70</i> mutation in P3, which is not included in the dbGaP submission. Autosomal recessive CD70 deficiency is a novel cause of combined immunodeficiency and EBV-associated diseases, reminiscent of CD27 deficiency.</p>

| phs001245 | dbGaP

CD70 identifies donor derived alloreactive T cells in severe acute Graft vs Host Disease post allogeneic SCT

Project description:Graft-versus-host disease (GvHD) remains a major challenge post allogeneic hematopoietic stem cell transplantation (allo-HSCT) and understanding its immunopathology is crucial for effective therapeutic intervention. Here we investigated the significance of CD70, a co-stimulatory molecule, in the context of aGvHD. CD70 was found to be transiently expressed on activated T cells during early immune reconstitution post-transplantation but persisted longer in aGvHD. Our findings illustrate that CD70+ T cells are characterized by upregulated activation receptors and enhanced cytokine production, while displaying signs of exhaustion. Remarkably, CD70+ T cells expressed chemokine receptors CCR4 and CCR6 and were actively recruited to inflamed tissues, implicating them in aGvHD pathogenesis. The chromatin at transcription factor MGA and NFAT5 loci was found to be selectively altered upon allo-antigenic stimulation in CD70+ T cells ex-vivo. Gene transcriptions of Toll-like receptors and MAPK signalling pathway were also found to differ in CD70+ and CD70- T cells of aGvHD patients. Insights into the clonality and antigen specificity of CD70+ T cell populations revealed potential novel antigenic targets. Further blocking CD70 in allogeneic T cells from aGvHD patients primed with autologous antigen presenting cells prior to HSCT demonstrated that anti-CD70 antibody reduced T cell proliferation and cytokine production. These findings implicate CD70 as a potential therapeutic target to modulate T cell responses and mitigate aGvHD. Targeting the CD70-CD27 co-stimulation pathway holds promise for prophylactic treatment.

2024-10-02 | GSE247452 | GEO

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