ArticleInfection and immunity2015
Protection from systemic Candida albicans infection by inactivation of the Sts phosphatases.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 38 citations in OpenAlex.
- Exploring UBASH3A: from immune regulation to autoimmune diseases.Journal of translational medicine · 2025Review
- Establishment and Validation of a Machine-Learning Prediction Nomogram Based on Lymphocyte Subtyping for Intra-Abdominal Candidiasis in Septic Patients.Clinical and translational science · 2025Article
- Rebamipide and Derivatives are Potent, Selective Inhibitors of Histidine Phosphatase Activity of the Suppressor of T Cell Receptor Signaling Proteins.Journal of medicinal chemistry · 2024Article
- TRIM26 alleviates fatal immunopathology by regulating inflammatory neutrophil infiltration during Candida infection.PLoS pathogens · 2024Article
- ThemSphere · 2023Article
- Article
- Inactivation of the Sts enzymes promotes resistance to lethalInfection and immunity · 2023Article
- Inflammatory ER stress responses dictate the immunopathogenic progression of systemic candidiasis.The Journal of clinical investigation · 2023Article
- TULA Proteins in Men, Mice, Hens, and Lice: Welcome to the Family.International journal of molecular sciences · 2023Review
- The Sts Proteins: Modulators of Host Immunity.International journal of molecular sciences · 2023Review
- Exploiting antifungal immunity in the clinical context.Seminars in immunology · 2023Review
- Fungal extracellular vesicle-mediated regulation: from virulence factor to clinical application.Frontiers in microbiology · 2023Review
- Pathogenesis and virulence ofVirulence · 2022Review
- De-coding genetic risk variants in type 1 diabetes.Immunology and cell biology · 2021Review
- A role for the Sts phosphatases in negatively regulating IFNγ-mediated production of nitric oxide in monocytes.Immunity, inflammation and disease · 2020Article
- Vaccination with Secreted Aspartyl Proteinase 2 Protein fromInfection and immunity · 2020Article
- An unexpected 2-histidine phosphoesterase activity of suppressor of T-cell receptor signaling protein 1 contributes to the suppression of cell signaling.The Journal of biological chemistry · 2020Article
- Stepping Up to the Plate(let) against Candida albicans.Infection and immunity · 2020Article
- Modulation of TCR Signaling by Tyrosine Phosphatases: From Autoimmunity to Immunotherapy.Frontiers in cell and developmental biology · 2020Review
- Discovery and Characterization of Two Classes of Selective Inhibitors of the Suppressor of the TCR Signaling Family of Proteins.ACS infectious diseases · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The human fungal pathogen Candida albicans causes invasive candidiasis, characterized by fatal organ failure due to disseminated fungal growth and inflammatory damage. The suppressor of TCR signaling 1 (Sts-1) and Sts-2 are two homologous phosphatases that negatively regulate signaling pathways in a number of hematopoietic cell lineages, including T lymphocytes, mast cells, and platelets. Functional inactivation of both Sts enzymes leads to profound resistance to systemic infection by C. albicans, such that greater than 80% of mice lacking Sts-1 and -2 survive a dose of C. albicans (2.5 × 10(5) CFU/mouse) that is uniformly lethal to wild-type mice within 10 days. Restriction of fungal growth within the kidney occurs by 24 h postinfection in the mutant mice. This occurs without induction of a hyperinflammatory response, as evidenced by the decreased presence of leukocytes and inflammatory cytokines that normally accompany the antifungal immune response. Instead, the absence of the Sts phosphatases leads to the rapid induction of a unique immunological environment within the kidney, as indicated by the early induction of a proinflammatory cytokine (CXL10). Mice lacking either Sts enzyme individually display an intermediate lethality phenotype. These observations identify an opportunity to optimize host immune responses toward a deadly fungal pathogen.
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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.