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Effect of depletion of LRIG1 on polyclonal CD8+ tumor infiltrating T cells and Effect of depletion of LRIG1 on OT1 CD8+ tumor-infiltrating T cells

ABSTRACT: Effect of depletion of LRIG1 on polyclonal CD8+ tumor infiltrating T cells and Effect of depletion of LRIG1 on OT1 CD8+ tumor-infiltrating T cells

PROVIDER: PRJNA1030053 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26445769_1.fastq.gz	Fastqsanger.gz
	SRR26445769_2.fastq.gz	Fastqsanger.gz
	SRR26445770_1.fastq.gz	Fastqsanger.gz
	SRR26445770_2.fastq.gz	Fastqsanger.gz
	SRR26445771_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of LRIG1 on polyclonal CD8+ tumor infiltrating T cells and Effect of depletion of LRIG1 on OT1 CD8+ tumor-infiltrating T cells

Project description:To investigate the function of LRIG11 in regulating the differentiation of polyclonal CD8 tumor infiltrating T cells during the response to B16melanoma. And, To investigate the function of LRIG1 in regulating the activaiton of ovalbumin specific OT1 CD8+ T cells during the response to B16 tumor stably expresss ovalbumin as surrogate tumor antigen.

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Effect of depletion of LRIG1 on CD8+ tumor infiltrating T cells

Project description:Effect of depletion of LRIG1 on CD8+ tumor infiltrating T cells

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Effect of depletion of LRIG1 on CD8+ tumor infiltrating T cells [CITE-Seq]

Project description:Effect of depletion of LRIG1 on CD8+ tumor infiltrating T cells [CITE-Seq]

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LRIG1 engages ligand VISTA and impairs tumor-specific CD8+ T cell responses

Project description:Cancer immunotherapies boost antitumor immunity and improve the survival of cancer patients. V-domain Immunoglobulin Suppressor of T cell Activation (VISTA) is an immune 20 checkpoint target but presents elusive signaling mechanisms. We report a novel VISTA binding partner, Leucine-Rich Repeats and Immunoglobulin Like Domains 1 (LRIG1), which acts as an inhibitory receptor by engaging VISTA and suppressing T cell receptor signaling pathways. Mice with T cell-specific LRIG1 deletion developed superior antitumor T cell responses. Mechanistically, LRIG1-deficient tumor-specific CD8+ cytotoxic T cells (CTLs) exhibited longer 25 persistence due to improved expansion and survival and greater effector function. Sustained tumor control was also associated with a reduction of quiescent CTLs (TCF1+ CD62Lhi PD-1low) and a reciprocal increase in progenitor and memory-like CTLs (TCF1+ PD-1+). In human melanoma, an elevated LRIG1 expression on tumor-infiltrating CD8+ CTLs correlated with resistance to immunotherapies. Taken together, these results delineate the role of LRIG1 as an inhibitory 30 immune checkpoint receptor and propose a rationale for targeting the VISTA/LRIG1 axis for cancer immunotherapy.

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Effect of depletion of LRIG1 on CD8+ tumor infiltrating T cells [CITE-Seq]

Project description:To investigate the function of LRIG11 in regulating the differentiation of polyclonal CD8 tumor infiltrating T cells during the response to B16melanoma, we isolated CD8 T cells on day 18 post vaccine treatment and examined gene transcription at single cell level

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Effect of depletion of LRIG1 on CD8+ tumor infiltrating T cells

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

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The transcriptomic effect of induced LRIG1 expression in NPC cells

Project description:As LRIG1 known to be a negative regulator of EGFR, we postulate that restored LRIG1 expression will change the transcription profile through the regulation of EGFR as well as its downstream signal cascades. Thus, we conducted a time-course microarray study to examine the effect of restored LRIG1 expression in NPC line, TW01-LG1/a, which the LRIG1 expression is under the control of a promoter with Doxycycline response element. We established stable transfectants of the LRIG1 gene in the TW01 cells which the expression of LRIG1 protein was barely detectable. To control the expression of LRIG1, the coding sequences were placed under the control of a promoter with doxycycline (Dox)-response element using the Tetoff system. Thus the LRIG1 expression could be turn on by removing Dox from the culture medium. Cellular total RNA were harvested along a time course of 12, 24, 36, and 48 hr following LRIG1 turn on expression, and then subjected to exon array analysis (Affymatrix Human Gene 1.0 ST), using the LRIG1 non-expressing sample (with Dox) as control for all comparison. For each time-point, a biological replicate was included.

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