ArticleJournal of immunology (Baltimore, Md. : 1950)2010
SHP-1 deficient mast cells are hyperresponsive to stimulation and critical in initiating allergic inflammation in the lung.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Decoding the shared genetic liability of lower respiratory tract infections via genomic structural equation modeling.BMC pulmonary medicine · 2026Article
- SHP-1 mediates cigarette smoke extract-induced epithelial-mesenchymal transformation and inflammation in 16HBE cells.Open medicine (Warsaw, Poland) · 2024Article
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- Article
- Aldh2 Attenuates Stem Cell Factor/Kit-Dependent Signaling and Activation in Mast Cells.International journal of molecular sciences · 2019Article
- Article
- Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice.Molecular medicine reports · 2019Article
- The Importance of Tyrosine Phosphorylation Control of Cellular Signaling Pathways in Respiratory Disease: pY and pY Not.American journal of respiratory cell and molecular biology · 2018Review
- Positive and Negative Regulatory Roles of C-Terminal Src Kinase (CSK) in FcεRI-Mediated Mast Cell Activation, Independent of the Transmembrane Adaptor PAG/CSK-Binding Protein.Frontiers in immunology · 2018Article
- Shp1 function in myeloid cells.Journal of leukocyte biology · 2017Review
- Protein tyrosine phosphatase SHP-1: resurgence as new drug target for human autoimmune disorders.Immunologic research · 2016Review
- Signal transduction and chemotaxis in mast cells.European journal of pharmacology · 2016Review
- Commentary: IL-4 and IL-13 receptors and signaling.Cytokine · 2015Article
- CD31 is a key coinhibitory receptor in the development of immunogenic dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- TRPA1-dependent pruritus in IL-13-induced chronic atopic dermatitis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- DJ-1 regulates mast cell activation and IgE-mediated allergic responses.The Journal of allergy and clinical immunology · 2013Article
- Distinct roles for neutrophils and dendritic cells in inflammation and autoimmunity in motheaten mice.Immunity · 2013Article
- Activation/Inhibition of mast cells by supra-optimal antigen concentrations.Cell communication and signaling : CCS · 2013Article
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- Interleukin-4- and interleukin-13-mediated alternatively activated macrophages: roles in homeostasis and disease.Annual review of immunology · 2013Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Phosphatase Src homology region 2 domain-containing phosphatase 1 (SHP-1)-deficient mice display an allergic asthma phenotype that is largely IL-13 and STAT6 dependent. The cell types responsible for the Th2 phenotype have not been identified. We hypothesized that SHP-1 deficiency leads to mast cell dysregulation and increased production and release of mediators and Th2 cytokines, leading to the allergic asthma phenotype. We examined SHP-1 regulation of mast cell differentiation, survival, and functional responses to stimulation using bone marrow-derived mast cells from viable motheaten (mev) mice. We assessed pulmonary phenotypical changes in mev mice on the mast cell-deficient Kit(W-Sh) genetic background. The results showed that SHP-1 deficiency led to increased differentiation and survival, but reduced proliferation, of mast cells. SHP-1-deficient mast cells produced and released increased amounts of mediators and Th2 cytokines IL-4 and -13 spontaneously and in response to H(2)O(2), LPS, and Fc epsilonI cross-linking, involving c-Kit-dependent and -independent processes. The Fc epsilonRI signaling led to binding of SHP-1 to linker for activation of T cells 2 and enhanced linker for activation of T cells 2 phosphorylation in mev bone marrow-derived mast cells. Furthermore, the number of mast cells in the lung tissue of mev mice was increased and mast cell production and release of Th2 cytokines were distinctly increased upon Fc epsilonRI stimulation. When backcrossed to the Kit(W-Sh) background, mev mice had markedly reduced pulmonary inflammation and Th2 cytokine production. These findings demonstrate that SHP-1 is a critical regulator of mast cell development and function and that SHP-1-deficient mast cells are able to produce increased Th2 cytokines and initiate allergic inflammatory responses in the lung.
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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.