ArticleThe American journal of pathology2011
Spontaneous insertion of a b2 element in the ptpn6 gene drives a systemic autoinflammatory disease in mice resembling neutrophilic dermatosis in humans.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Redundant γc cytokines license IL-1-driven neutrophil inflammation through MEK/ERK convergence.bioRxiv : the preprint server for biology · 2026Article
- PTPN6/SHP-1 in autoimmune disease: immune tolerance, regulatory mechanisms, and therapeutic targeting.Frontiers in immunology · 2026Review
- Innate Immune Sensors and Cell Death-Frontiers Coordinating Homeostasis, Immunity, and Inflammation in Skin.Viruses · 2025Review
- Loss of neutrophil Shp1 produces hemorrhagic and lethal acute lung injury.bioRxiv : the preprint server for biology · 2024Article
- The Pathophysiology and Treatment of Pyoderma Gangrenosum-Current Options and New Perspectives.International journal of molecular sciences · 2024Review
- SHP-1 Protein Tyrosine Phosphatase Affects Early Postnatal Bone Development in Mice.Calcified tissue international · 2023Article
- CD47 haltsScience advances · 2023Article
- Pyoderma Gangrenosum: An Updated Literature Review on Established and Emerging Pharmacological Treatments.American journal of clinical dermatology · 2022Review
- [Research advances on the pathogenesis and diagnosis of pyoderma gangrenosum].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2022Review
- Hereditable variants of classical protein tyrosine phosphatase genes: Will they prove innocent or guilty?Frontiers in cell and developmental biology · 2022Review
- Analysis of SINE Families B2, Dip, and Ves with Special Reference to Polyadenylation Signals and Transcription Terminators.International journal of molecular sciences · 2021Article
- Ets-2 deletion in myeloid cells attenuates IL-1α-mediated inflammatory disease caused by a Ptpn6 point mutation.Cellular & molecular immunology · 2021Article
- Immune-Mediated Dermatoses in Patients with Haematological Malignancies: A Comprehensive Review.American journal of clinical dermatology · 2020Review
- Pyoderma gangrenosum.Nature reviews. Disease primers · 2020Review
- Regulation of autoimmune arthritis by the SHP-1 tyrosine phosphatase.Arthritis research & therapy · 2020Article
- Inflammasomes in the pathophysiology of autoinflammatory syndromes.Journal of leukocyte biology · 2020Review
- KLICK Syndrome Linked to aFrontiers in immunology · 2020Review
- Shp1 Loss Enhances Macrophage Effector Function and Promotes Anti-Tumor Immunity.Frontiers in immunology · 2020Article
- Mouse germ line mutations due to retrotransposon insertions.Mobile DNA · 2019Review
- Insights Into the Pathogenesis of Sweet's Syndrome.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We found a spontaneous autosomal mutation in a mouse leading to neutrophil infiltration with ulceration in the upper dermis of homozygous offspring. These animals had increased neutrophil numbers, associated with normal lymphocyte count, in peripheral blood and bone marrow, suggesting a myeloproliferative disorder; however, granulocyte precursor proliferation in bone marrow was actually reduced (because circulating neutrophils were less susceptible to apoptosis). Neutrophil infiltration of the skin and other organs and high serum levels of immunoglobulins and autoantibodies, cytokines, and acute-phase proteins were additional abnormalities, all of which could be reduced by high-dose corticosteroid treatment or neutrophil depletion by antibodies. Use of genome-wide screening localized the mutation within an 0.4-Mbp region on mouse chromosome 6. We identified insertion of a B2 element in exon 6 of the Ptpn6 gene (protein tyrosine phosphatase, non-receptor type 6; also known as Shp-1). This insertion involves amino acid substitutions that significantly reduced the enzyme activity in mice homozygous for the mutation. Disease onset was delayed, and the clinical phenotype was milder than the phenotypes of other Ptpn6-mutants described in motheaten (me, mev) mice; we designated this new genotype as Ptpn6(meB2/meB2) and the phenotype as meB2. This new phenotype encompasses an autoinflammatory disease showing similarities to many aspects of the so-called neutrophilic dermatoses, a heterogeneous group of skin diseases with unknown etiology in humans.
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