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Programmed cell death-1 receptor deficiency enhances CD30+ T regulatory cell function in Melanoma [Murine scRNAseq]

ABSTRACT: Programmed cell death-1 receptor deficiency enhances CD30+ T regulatory cell function in Melanoma [Murine scRNAseq]

PROVIDER: PRJNA1142058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30046136_1.fastq.gz	Fastqsanger.gz
	SRR30046136_2.fastq.gz	Fastqsanger.gz

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Programmed cell death-1 receptor deficiency enhances CD30+ T regulatory cell function in Melanoma [Murine scRNAseq]

Project description:Regulatory T cells (Tregs) are vital for immune suppression rendering their function through multiple pathways including the expression of co-inhibitory receptors. The role of co-receptors namely PD1 in Treg function remains controversial. We demonstrate that PD1 is a master checkpoint in Tregs controlling several aspects of Treg biology in tumor immunity. Our data demonstrates that PD1 controls the expression and function of a unique co-inhibitory receptor network that dictates Treg function. We found that CD30 plays a central role within this network in driving Treg suppressive function within the tumor microenvironment (TME). Mechanistically, PD1 deficiency unleashed enhanced STAT5 signaling in Tregs, which drove CD30 expression. Our work highlights a new role for PD1 as a checkpoint that negatively controls CD30 expression in Tregs thereby dampening their function. Understanding the landscape changes that PD1 renders to Treg function can enable the use of combination therapies for better treatment outcomes in cancer.

2025-04-09 | GSE273532 | GEO

Programmed cell death-1 receptor deficiency enhances CD30+ T regulatory cell function in Melanoma [Murine NanoString CosMx SMI]

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Programmed cell death-1 receptor deficiency enhances CD30+ T regulatory cell function in Melanoma [Murine NanoString CosMx SMI]

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Beyond CD30 Targeting: Brentuximab Vedotin Triggers Immunogenic Cell Death and Antitumor Immunity in Mycosis Fungoides, Overcoming Resistance via BCL2 Inhibition

Project description:Background: Mycosis fungoides (MF), the most common subtype of cutaneous T cell lymphoma (CTCL), has poor prognosis in advanced stages due to lack of effective therapies. Brentuximab vedotin (BV), an antigen-drug conjugate targeting CD30, is approved for CD30+ MF after prior systemic treatment. However, many patients develop resistance with unclarified mechanisms. Method: We conducted single-cell RNA sequencing on 13 paired tumor samples from 6 CD30+ MF patients treated with BV. Eight post-treatment samples were grouped into responsive (n = 5) and non-responsive (n = 3) lesions based on pathologic response. Combination effects of BV and BCL2 inhibitors were assessed in CD30+ CTCL cell lines. Result: BV induced immunogenic cell death (ICD) in both CD30+ and CD30- malignant T cells, enhancing their MHC-II-mediated antigen presentation in responsive lesions. Besides, BV specifically enhanced the IFNα/γ responses in CD30- malignant T cells. These coincided with TME reprogramming: diminished immunosuppressive function of Tregs and activated antitumor immunity mediated by dendritic cells, CD8+ T and NK cells. In non-responsive lesions, resistance was driven by distinct mechanisms: CD30+ malignant T cells upregulated the drug efflux transporter ABCB1 and exhibited impaired endosomal processing, while CD30- tumor cells overexpressed the anti-apoptotic protein BCL2 and displayed blunted IFN response. We confirmed potent synergy between BV and BCL2 inhibitors in CTCL cell lines, overcoming resistance. Conclusion: Beyond direct CD30+ targeting, BV transforms the immunosuppressive milieu by inducing ICD in tumor cells and suppressing Tregs. Resistance involves ABCB1 upregulation in CD30+ cells and BCL2-mediated survival in CD30- cells. Combining BV with BCL2 inhibitors represents a promising strategy to overcome resistance in CD30+ CTCL.

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