ArticleEuropean journal of immunology2012
Lineage extrinsic and intrinsic control of immunoregulatory cell numbers by SHIP.
Article in European journal of immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed.
- SHIP1 is required for T cell surveillance of occult malignancies.Cellular and molecular life sciences : CMLS · 2026Article
- Obesity control by SHIP inhibition requires pan-paralog inhibition and an intact eosinophil compartment.iScience · 2023Article
- Inhibition of lipid phosphatase SHIP1 expands myeloid-derived suppressor cells and attenuates rheumatoid arthritis in mice.American journal of physiology. Cell physiology · 2021Article
- Selective deletion of SHIP-1 in hematopoietic cells in mice leads to severe lung inflammation involving ILC2 cells.Scientific reports · 2021Article
- MicroRNA-21 and microRNA-155 promote the progression of Burkitt's lymphoma by the PI3K/AKT signaling pathway.International journal of clinical and experimental pathology · 2020Article
- Erythropoietin, a multifaceted protein with innate and adaptive immune modulatory activity.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019Review
- Loss of lipid phosphatase SHIP1 promotes macrophage differentiation through suppression of dendritic cell differentiation.Cancer biology & therapy · 2019Article
- Targeting SHIP-1 in Myeloid Cells Enhances Trained Immunity and Boosts Response to Infection.Cell reports · 2018Article
- Expression of microRNA-155 in inflammatory cells modulates liver injury.Hepatology (Baltimore, Md.) · 2018Article
- Interleukin 4 promotes the development of ex-Foxp3 Th2 cells during immunity to intestinal helminths.The Journal of experimental medicine · 2017Article
- Phenotype, development, and biological function of myeloid-derived suppressor cells.Oncoimmunology · 2016Review
- Host miR155 promotes tumor growth through a myeloid-derived suppressor cell-dependent mechanism.Cancer research · 2015Article
- Impaired T-cell survival promotes mucosal inflammatory disease in SHIP1-deficient mice.Mucosal immunology · 2014Article
- SHIP1 regulates MSC numbers and their osteolineage commitment by limiting induction of the PI3K/Akt/β-catenin/Id2 axis.Stem cells and development · 2014Article
- Discovery and development of small molecule SHIP phosphatase modulators.Medicinal research reviews · 2014Review
- SHIP-1 deficiency in the myeloid compartment is insufficient to induce myeloid expansion or chronic inflammation.Genes and immunity · 2014Article
- Milk: an exosomal microRNA transmitter promoting thymic regulatory T cell maturation preventing the development of atopy?Journal of translational medicine · 2014Review
- Role of inositol poly-phosphatases and their targets in T cell biology.Frontiers in immunology · 2013Review
- Pharmacological targeting of phosphoinositide lipid kinases and phosphatases in the immune system: success, disappointment, and new opportunities.Frontiers in immunology · 2012Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
We previously showed that germline or induced SHIP deficiency expands immuno-regulatory cell numbers in T lymphoid and myeloid lineages. We postulated these increases could be interrelated. Here, we show that myeloid-specific ablation of SHIP leads to the expansion of both myeloid-derived suppressor cell (MDSC) and regulatory T (Treg) cell numbers, indicating SHIP-dependent control of Treg-cell numbers by a myeloid cell type. Conversely, T-lineage specific ablation of SHIP leads to expansion of Treg-cell numbers, but not expansion of the MDSC compartment, indicating SHIP also has a lineage intrinsic role in limiting Treg-cell numbers. However, the SHIP-deficient myeloid cell that promotes MDSC and Treg-cell expansion is not an MDSC as they lack SHIP protein expression. Thus, regulation of MDSC numbers in vivo must be controlled in a cell-extrinsic fashion by another myeloid cell type. We had previously shown that G-CSF levels are profoundly increased in SHIP(-/-) mice, suggesting this myelopoietic growth factor could promote MDSC expansion in a cell-extrinsic fashion. Consistent with this hypothesis, we find that G-CSF is required for expansion of the MDSC splenic compartment in mice rendered SHIP-deficient as adults. Thus, SHIP controls MDSC numbers, in part, by limiting production of the myelopoietic growth factor G-CSF.
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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.