ArticleRare diseases (Austin, Tex.)2014
SHP-1 and IL-1α conspire to provoke neutrophilic dermatoses.
Article in Rare diseases (Austin, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Redundant γc cytokines license IL-1-driven neutrophil inflammation through MEK/ERK convergence.bioRxiv : the preprint server for biology · 2026Article
- Article
- 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
- Pyoderma Gangrenosum: An Updated Literature Review on Established and Emerging Pharmacological Treatments.American journal of clinical dermatology · 2022Review
- Pyoderma gangrenosum.Nature reviews. Disease primers · 2020Review
- Improved mouse models and advanced genetic and genomic technologies for the study of neutrophils.Drug discovery today · 2020Review
- Evidence for a role of autoinflammation in early-phase psoriasis.Clinical and experimental immunology · 2019Article
- Mechanisms of Inflammation in Neutrophil-Mediated Skin Diseases.Frontiers in immunology · 2019Review
- Cutting Edge: Dysregulated CARD9 Signaling in Neutrophils Drives Inflammation in a Mouse Model of Neutrophilic Dermatoses.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- ASK1/2 signaling promotes inflammation in a mouse model of neutrophilic dermatosis.The Journal of clinical investigation · 2018Article
- A Comprehensive Review of Neutrophilic Diseases.Clinical reviews in allergy & immunology · 2018Review
- Pyoderma gangrenosum-a novel approach?Wiener medizinische Wochenschrift (1946) · 2017Review
- Distinct role of IL-1β in instigating disease in SharpinScientific reports · 2016Article
- Protein tyrosine phosphatase SHP-1: resurgence as new drug target for human autoimmune disorders.Immunologic research · 2016Review
- Emerging Roles for the Immune System in Traumatic Brain Injury.Frontiers in immunology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Neutrophilic dermatoses are a spectrum of autoinflammatory skin disorders that are characterized by extensive infiltration of neutrophils into the epidermis and dermis. The underlining biological pathways that are responsible for this heterogeneous group of cutaneous diseases have remained elusive. However, recent work from our laboratory and other groups has shown that missense mutations in Ptpn6, which encodes for the non-receptor protein tyrosine phosphatase Src homology region 2 (SH2) domain-containing phosphatase-1 (SHP-1), results in a skin disease with many of the major histopathological and clinical features that encompass neutrophilic dermatoses in humans. In particular, we found that loss-of-function mutation in Ptpn6 results in unremitting footpad swelling, suppurative inflammation, and neutrophilia. Dysregulated wound healing responses were discovered to contribute to chronic inflammatory skin disease in SHP-1 defective mice and genetic abrogation of interleukin-1 receptor (IL-1R) protected mice from cutaneous inflammation, suggesting that IL-1-mediated events potentiate disease. Surprisingly, inflammasome activation and IL-1β-mediated events were dispensable for Ptpn6(spin) -mediated footpad disease. Instead, RIP1-mediated regulation of IL-1α was identified to be the major driver of inflammation and tissue damage.
Indexed as
Identifiers
What OpenQuestion holds
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.