ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Loss of the Protein Tyrosine Phosphatase PTPN22 Reduces Mannan-Induced Autoimmune Arthritis in SKG Mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- The protein tyrosine phosphatase Lyp/PTPN22 drives TNFα-induced priming of superoxide anions production by neutrophils and arthritis.Free radical biology & medicine · 2025Article
- Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025Review
- Autoimmunity-associated allele of tyrosine phosphatase gene PTPN22 enhances anti-viral immunity.PLoS pathogens · 2024Article
- Regulation of T Cell Signaling and Immune Responses by PTPN22.Molecular and cellular biology · 2024Review
- Targeting protein phosphatases in cancer immunotherapy and autoimmune disorders.Nature reviews. Drug discovery · 2023Review
- Genetic Polymorphism ofMedicina (Kaunas, Lithuania) · 2022Review
- Overexpression of theJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.PloS one · 2021Article
- LACC1 Regulates TNF and IL-17 in Mouse Models of Arthritis and Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Protein tyrosine phosphatase PTPN22 regulates LFA-1 dependent Th1 responses.Journal of autoimmunity · 2018Article
- Genetics of immune-mediated inflammatory diseases.Clinical and experimental immunology · 2018Review
- Regulation of autoimmune and anti-tumour T-cell responses by PTPN22.Immunology · 2018Review
- ZAP-70 in Signaling, Biology, and Disease.Annual review of immunology · 2018Review
- Crispr/Cas Mediated Deletion of PTPN22 in Jurkat T Cells Enhances TCR Signaling and Production of IL-2.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The cytoplasmic phosphatase, protein tyrosine phosphatase nonreceptor type 22 (PTPN22), is a negative regulator of T cell signaling. Genome-wide association studies have shown that single-nucleotide polymorphisms in PTPN22 confer an increased risk of developing multiple autoimmune diseases in humans. The precise function of PTPN22 and how the variant protein contributes to autoimmunity is not well understood. To address this issue, we investigated the effect of PTPN22 deficiency on disease susceptibility in a mouse model of autoimmune arthritis. The SKG mouse expresses a hypomorphic mutant allele of ZAP70, which, upon exposure to fungal Ags, predisposes the mice to a CD4(+) T cell-mediated autoimmune arthritis that closely resembles rheumatoid arthritis in humans. Surprisingly, SKG Ptpn22(-/-) mice developed less severe mannan-induced arthritis compared with SKG mice. Diminution of disease was not due to significant alterations in thymocyte development or repertoire selection in SKG Ptpn22(-/-) mice, even though T cell-mediated signal transduction was improved. Instead, Ptpn22 deficiency appeared to bias CD4 Th cell differentiation away from the Th17 lineage, which is pathogenic in this setting, to a more Th1/T regulatory-focused response. These data show that even small perturbations in TCR signal transduction pathways can have profound consequences on the differentiation of T cell lineages and thus for the development of autoimmune diseases.
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Registered trials
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