ArticleThe Journal of clinical investigation2011
Unraveling the functional implications of GWAS: how T cell protein tyrosine phosphatase drives autoimmune disease.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Identification of the tyrosine-protein phosphatase non-receptor type 2 as a rheumatoid arthritis susceptibility locus in europeans.PloS one · 2013Pooled it
- Deletion of Ptpn2 in B cells promotes autoimmunity via TLR and JAK/STAT signaling.JCI insight · 2025Article
- The phosphatases TCPTP, PTPN22, and SHP1 play unique roles in T cell phosphotyrosine maintenance and feedback regulation of the TCR.Scientific reports · 2025Article
- α-Methyl-Tryptophan Inhibits SLC6A14 Expression and Exhibits Immunomodulatory Effects in Crohn's Disease.Journal of inflammation research · 2025Article
- Protein tyrosine phosphatase non-receptor type 2 (PTPN2) gene polymorphisms (rs2542151, rs7234029) in Egyptian Behçet's disease patients: a preliminary report.Clinical rheumatology · 2024Article
- Inflammation versus regulation: how interferon-gamma contributes to type 1 diabetes pathogenesis.Frontiers in cell and developmental biology · 2023Review
- Common polymorphisms of protein tyrosine phosphate non-receptor type 2 gene are not associated with risk of Crohn's disease in Indian.World journal of gastrointestinal pathophysiology · 2022Article
- Modulation ofInternational journal of molecular sciences · 2021Article
- PTPN2 Deficiency Enhances Programmed T Cell Expansion and Survival Capacity of Activated T Cells.Cell reports · 2020Article
- Efficient CRISPR/Cas9 Disruption of Autoimmune-Associated Genes Reveals Key Signaling Programs in Primary Human T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- PTPN2 improved renal injury and fibrosis by suppressing STAT-induced inflammation in early diabetic nephropathy.Journal of cellular and molecular medicine · 2019Article
- Double-negative T cells remarkably promote neuroinflammation after ischemic stroke.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- An allelic variant in the intergenic region between ERAP1 and ERAP2 correlates with an inverse expression of the two genes.Scientific reports · 2018Article
- Role ofWorld journal of gastroenterology · 2018Article
- The tyrosine phosphatase PTPN22 discriminates weak self peptides from strong agonist TCR signals.Nature immunology · 2014Article
- Network analysis identifies protein clusters of functional importance in juvenile idiopathic arthritis.Arthritis research & therapy · 2014Article
- Pathogenesis and prevention of rheumatic disease: focus on preclinical RA and SLE.Nature reviews. Rheumatology · 2014Review
- Can rheumatoid arthritis be prevented?Best practice & research. Clinical rheumatology · 2013Review
- Pre-rheumatoid arthritis: predisposition and transition to clinical synovitis.Nature reviews. Rheumatology · 2012Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Genome-wide association studies (GWAS) have identified a large number of SNPs that are linked to human autoimmune diseases. However, the functional consequences of most of these genetic variations remain undefined. T cell protein tyrosine phosphatase (TCPTP, which is encoded by PTPN2) is a JAK/STAT and growth factor receptor phosphatase that has been linked to the pathogenesis of type 1 diabetes, rheumatoid arthritis, and Crohn's disease by GWAS. In this issue of the JCI, Wiede and colleagues have generated a T cell-specific deletion of TCPTP and identified a novel role for this phosphatase as a negative regulator of TCR signaling. These data provide new insight as to how noncoding PTPN2 SNPs identified in GWAS could drive human autoimmune diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.