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The roles of Ptpn22 Ser452 phosphorylation in tumor-infiltrating CD8+ T cells from mouse

ABSTRACT: The roles of Ptpn22 Ser452 phosphorylation in tumor-infiltrating CD8+ T cells from mouse

PROVIDER: PRJNA1095827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28538346_1.fastq.gz	Fastqsanger.gz
	SRR28538346_2.fastq.gz	Fastqsanger.gz
	SRR28538347_1.fastq.gz	Fastqsanger.gz
	SRR28538347_2.fastq.gz	Fastqsanger.gz
	SRR28538348_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The roles of Ptpn22 Ser452 phosphorylation in tumor-infiltrating CD8+ T cells from mouse

Project description:Protein Tyrosine Phosphatase Non-receptor type 22 (PTPN22) is encoded by a major autoimmunity gene and is a known inhibitor of T cell receptor (TCR) signaling for cancer immunotherapy. However, little is known about PTPN22 phosphorylation in tumor infiltrating T cells. Here we characterize a phosphorylation site at Ser452 situated in the interdomain of PTPN22, and its roles in altering T cell function and tumor growth. Tumor infiltrating CD8+ T cells from PepWT or PepS452A mice were collected and subjected to next-generation sequencing (NGS). The results revealed it differentially regulates the genes expression of metabolic process, cytokine prodcution and adaptive immunity etc. This study explores the function of a novel phosphorylation site of PTPN22 that is involved in complex regulation of CD8+ T cell activity, fuctions and tumor growth.

2025-04-02 | GSE263092 | GEO

A novel gain-of-function phosphorylation site modulates PTPN22 inhibition of TCR signaling

Project description:Protein Tyrosine Phosphatase Non-receptor type 22 (PTPN22) is encoded by a major autoimmunity gene and is a known inhibitor of T cell receptor (TCR) signaling and drug target for cancer immunotherapy. However, little is known about PTPN22 post-translational regulation. Here we characterize a phosphorylation site at Ser325 situated C-terminal to the catalytic domain of PTPN22, and its roles in altering protein function. Signaling through the major TCR-dependent pathway under PTPN22 control was enhanced by CRISPR/Cas9 mediated suppression of Ser325 phosphorylation and inhibited by mimicking it via glutamic acid substitution. Next-generation sequencing (NGS) revealed it differentially regulates the expression of chemokines and T cell activation pathways. In conclusion, this study explores the function of a novel phosphorylation site of PTPN22 that is involved in complex regulation of TCR signaling .

2024-07-17 | GSE264373 | GEO

Phosphorylation sites of PTPN22 treated by Calyculin A in 293T cells

Project description:Phosphorylation sites of PTPN22 induced by Calyculin A treatment were identified by LC-MS

2021-09-08 | PXD016103 | Pride

Gene expression profiles at single cell level of nucleotides optimized WT or S449A PTPN22 in J.Lck WT or J.Lck Y192F Jurkat cells

Project description:Protein Tyrosine Phosphatase Non-receptor type 22 (PTPN22) is encoded by a major autoimmunity gene and is a known inhibitor of T cell receptor (TCR) signaling. PTPN22 Ser449 is a novel phosphorylation site. Here we used optimized coding sequences (CDS) of PTPN22 WT or S449A eukaryotic expression vectors with N-terminal mEGFP and electroporated into either J.Lck WT or J.Lck Y192F cells to analyze the relationship between PTPN22 Ser449 phosphorylaion and Lck Tyr192 phosphorylaion by CITE seq.

2025-04-25 | GSE265961 | GEO

A novel gain-of-function phosphorylation site modulates PTPN22 inhibition of TCR signaling

Project description:A novel gain-of-function phosphorylation site modulates PTPN22 inhibition of TCR signaling

| PRJNA1102292 | ENA

Expression data from FACS-sorted CD8+BTLA+ vs CD8+BTLA- Human Tumor-infiltrating Lymphocytes in Metastatic Melanoma

Project description:Adoptive T-cell Therapy (ACT) involves using tumor-infiltrating lymphocytes (TIL) isolated from metastatic melanoma and expanding them ex vivo prior to infusion into lympho-depleted patients. This is one of the most promising approaches to treat metastatic melanoma, with the rates of clinical response between 48-50% based on studies done at NCI, M.D. Anderson Cancer Center (Houston, TX), and Sheba Medical Center (Tel Aviv, Israel). In the Phase II ACT Trial at M.D. Anderson Cancer Center , our group has uncovered an association between positive clinical response and the amount of CD8+ tumor-infiltrating lymphocytes expressing B and T Lymphocyte Attenuator (BTLA), a reported inhibitory receptor on T-cells. We used microarrays to detail the differences in the global programme of gene expression between CD8+BTLA+ vs CD8+BTLA- TILs in order to understand the molecular basis of the clinical association. TILs were isolated by enzymatically digest the melanoma tumor fragments obtained from Stage IIIc/IV melanoma patients at M.D. Anderson Cancer Center. The TILs were expanded with high-dose IL-2 for two weeks prior to sorting by FACS (fluoresecence-activated cell sorter) for CD8+BTLA+ and CD8+BTLA- susbets. RNA was extracted from each sorted subsets and hybridized on Affymetrix microarrays

2013-01-03 | E-GEOD-43260 | biostudies-arrayexpress

PTPN22 autoimmune susceptibility gene affects the removal of human developing autoreactive B cells

Project description:Protein tyrosine phosphatase nonreceptor type 22 (PTPN22) gene segregates with most autoimmune diseases; its risk allele encodes overactive PTPN22 phosphatases that alter B cell receptor (BCR) signaling potentially involved in the regulation of central B cell tolerance. To assess whether PTPN22 risk allele affects the removal of developing autoreactive B cells, we tested by ELISA the reactivity of recombinant antibodies isolated from single B cells from asymptomatic healthy individuals carrying one or two PTPN22 risk allele(s). We found that new emigrant/transitional and mature naive B cells from PTPN22 risk allele carriers contained high frequencies of autoreactive clones compared to non-carrier control donors. Hence, a single PTPN22 risk allele has a dominant effect on altering autoreactive B cell counterselection, suggesting that early B cell tolerance checkpoint defects precede the onset of autoimmunity. In addition, gene array experiments comparing mature naïve B cells from healthy individuals carrying or not PTPN22 risk allele(s) revealed that the strength of association of PTPN22 for autoimmunity, second in importance only to the MHC, may not only be due to BCR signaling alteration but also to the regulation of other genes, which themselves have also been identified as involved in the development of autoimmune diseases. The PTPN22 risk allele is a single nucleotide change (cytidine to thymidine) at residue 1858, which results in a single amino acid substitution from arginine to tryptophan at position 620 of the PTPN22/Lyp protein.

2010-10-16 | GSE24736 | GEO

Immunoprecipitated PTPN22 Phosphoproteomics from Jurkat Cells

Project description:3x FLAG tagged PTPN22 were immunoprecipitated from Jurkat cells stimulated by TCR for 5min, and the proteins were eluted by FLAG peptides. This study aims to explore the phosphorylation sites on PTPN22 phosphatase, identifying two phosphorylation sites Ser325 and Ser449.

2023-12-21 | MSV000093717 | MassIVE

EOMES-expressing CD4+ T cells are increased in PTPN22 (1858T) risk allele carriers

Project description:The presence of the PTPN22 risk variant (1858T) is associated to several autoimmune diseases including rheumatoid arthritis (RA). Despite a number of studies exploring the function of PTPN22 in T cells, the exact impact of the PTPN22 risk variant on T cell function in humans is still unclear. In this study, using RNA sequencing, we show that, upon TCR-activation, naïve CD4+ T cells carrying two PTPN22 risk alleles overexpress a limited number of genes including CFLAR and 4-1BB important for cytotoxic T cell differentiation. Moreover, an increased number of cytotoxic EOMES+ CD4+ T cells were observed in PTPN22 risk allele carriers, which negatively correlated with a decreased number of naïve T cells in older individuals. No difference in the frequency of other CD4+ T cell subsets (Th1, Th17, Tfh, Treg) was observed in PTPN22 risk allele carriers and Treg suppressive capacity was not altered. Finally, in synovial fluids of RA patients, an accumulation of EOMES+ CD4+ T cells was observed with a more pronounced production of Perforin-1 in PTPN22 risk allele carriers. Altogether, our data provide a novel mechanism of action of PTPN22 risk variant on CD4+ T-cell differentiation and identify EOMES+ CD4+ T cell as a relevant T cell subset in RA.

2018-02-27 | GSE94859 | GEO

PTPN22 microbiota

Project description:Association of PTPN22 genotype to the murine gut microbiota

| PRJEB26758 | ENA