ArticlePloS one2014
Chronic proliferative dermatitis in Sharpin null mice: development of an autoinflammatory disease in the absence of B and T lymphocytes and IL4/IL13 signaling.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Early Development of Ocadusertib, a Selective Receptor-Interacting Serine/Threonine-Protein Kinase 1 Inhibitor.Clinical and translational science · 2026Trial
- SHARPIN restrains IL-33 release by stromal cells to control ILC2 inflammation.Science advances · 2026Article
- Myofiber-type-dependent 'boulder' or 'multitudinous pebble' formations across distinct amylopectinoses.Acta neuropathologica · 2024Article
- Preclinical Models of Atopic Dermatitis Suitable for Mechanistic and Therapeutic Investigations.Journal of inflammation research · 2024Review
- Mind bomb 2 limits inflammatory dermatitis inPNAS nexus · 2024Article
- Characterization of SHARPIN knockout Syrian hamsters developed using CRISPR/Cas9 system.Animal models and experimental medicine · 2023Article
- Repressive Control of Keratinocyte Cytoplasmic Inflammatory Signaling.International journal of molecular sciences · 2023Review
- SHARPIN: Role in Finding NEMO and in Amyloid-Beta Clearance and Degradation (ABCD) Pathway in Alzheimer's Disease?Cellular and molecular neurobiology · 2022Review
- Platelet SHARPIN regulates platelet adhesion and inflammatory responses through associations with αIIbβ3 and LUBAC.Blood advances · 2022Article
- RIP1 kinase activity is critical for skin inflammation but not for viral propagation.Journal of leukocyte biology · 2020Article
- Full-term low birth weight infants have differentially hypermethylated DNA related to immune system and organ growth: a comparison with full-term normal birth weight infants.BMC research notes · 2020Article
- SHARPIN Inhibits Esophageal Squamous Cell Carcinoma Progression by Modulating Hippo Signaling.Neoplasia (New York, N.Y.) · 2020Article
- Keratinocyte-specific deletion of SHARPIN induces atopic dermatitis-like inflammation in mice.PloS one · 2020Article
- The Balance of TNF Mediated Pathways Regulates Inflammatory Cell Death Signaling in Healthy and Diseased Tissues.Frontiers in cell and developmental biology · 2020Review
- Modulation of autoimmune pathogenesis by T cell-triggered inflammatory cell death.Nature communications · 2019Article
- E3 ubiquitin ligases in B-cell malignancies.Cellular immunology · 2019Review
- SHARPIN at the nexus of integrin, immune, and inflammatory signaling in human platelets.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Profiling of epidermal lipids in a mouse model of dermatitis: Identification of potential biomarkers.PloS one · 2018Article
- Loss of FAS/FASL signalling does not reduce apoptosis in Sharpin null mice.Experimental dermatology · 2017Article
- MicroRNA differential expression spectrum and microRNA-125a-5p inhibition of laryngeal cancer cell proliferation.Experimental and therapeutic medicine · 2017Article
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9 authors at 2 institutions in 1 country.
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Abstract
SHARPIN is a key regulator of NFKB and integrin signaling. Mice lacking Sharpin develop a phenotype known as chronic proliferative dermatitis (CPDM), typified by progressive epidermal hyperplasia, apoptosis of keratinocytes, cutaneous and systemic eosinophilic inflammation, and hypoplasia of secondary lymphoid organs. Rag1(-/-) mice, which lack mature B and T cells, were crossed with Sharpin(-/-) mice to examine the role of lymphocytes in CDPM. Although inflammation in the lungs, liver, and joints was reduced in these double mutant mice, dermatitis was not reduced in the absence of functional lymphocytes, suggesting that lymphocytes are not primary drivers of the inflammation in the skin. Type 2 cytokine expression is increased in CPDM. In an attempt to reduce this aspect of the phenotype, Il4ra(-/-) mice, unresponsive to both IL4 and IL13, were crossed with Sharpin(-/-) mice. Double homozygous Sharpin(-/-) , Il4ra(-/-) mice developed an exacerbated granulocytic dermatitis, acute system inflammation, as well as hepatic necrosis and mineralization. High expression of CHI3L4, normally seen in CPDM skin, was abolished in Sharpin(-/-) , Il4ra(-/-) double mutant mice indicating the crucial role of IL4 and IL13 in the expression of this protein. Cutaneous eosinophilia persisted in Sharpin(-/-) , Il4ra(-/-) mice, although expression of Il5 mRNA was reduced and the expression of Ccl11 and Ccl24 was completely abolished. TSLP and IL33 were both increased in the skin of Sharpin(-/-) mice and this was maintained in Sharpin(-/-) , Il4ra(-/-) mice suggesting a role for TSLP and IL33 in the eosinophilic dermatitis in SHARPIN-deficient mice. These studies indicate that cutaneous inflammation in SHARPIN-deficient mice is autoinflammatory in nature developing independently of B and T lymphocytes, while the systemic inflammation seen in CPDM has a strong lymphocyte-dependent component. Both the cutaneous and systemic inflammation is enhanced by loss of IL4 and IL13 signaling indicating that these cytokines normally play an anti-inflammatory role in SHARPIN-deficient mice.
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