ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Expression and functional significance of SOCS-1 and SOCS-3 in astrocytes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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
76 citing papers in PubMed, 126 citations in OpenAlex.
- Pervasive Somatic Mutations inbioRxiv : the preprint server for biology · 2026Article
- Post-translational modifications in Neuroimmune cells during neuroinflammation: integrated regulatory networks and therapeutic opportunities.Biology direct · 2026Review
- An Update Comprehensive Review on Epigenetic Modifications and Therapies in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2026Review
- New insight into the role of SOCS family in immune regulation and autoimmune pathogenesis.Journal of advanced research · 2026Review
- Article
- Rewired type I IFN signaling is linked to age-dependent differences in COVID-19.Cell reports. Medicine · 2025Article
- The Impact of Innate Components on Viral Pathogenesis in the Neurotropic Coronavirus Encephalomyelitis Mouse Model.Viruses · 2023Review
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- Aging, Plasminogen Activator Inhibitor 1, Brain Cell Senescence, and Alzheimer's Disease.Aging and disease · 2023Article
- Review
- The role of non-coding RNAs in neuroinflammatory process in multiple sclerosis.Molecular neurobiology · 2022Review
- Application of Sensitivity Analysis to Discover Potential Molecular Drug Targets.International journal of molecular sciences · 2022Article
- FTO Suppresses STAT3 Activation and Modulates Proinflammatory Interferon-Stimulated Gene Expression.Journal of molecular biology · 2022Article
- Article
- Bu Shen Yi Sui Capsule Promotes Myelin Repair by Modulating the Transformation of A1/A2 Reactive AstrocytesOxidative medicine and cellular longevity · 2022Article
- The gamble between oncolytic virus therapy and IFN.Frontiers in immunology · 2022Review
- IL-17A Mediates Demyelination by Activating A1 AstrocytesFrontiers in immunology · 2022Article
- SOCS proteins and their roles in the development of glioblastoma.Oncology letters · 2022Review
- Glial and myeloid heterogeneity in the brain tumour microenvironment.Nature reviews. Cancer · 2021Review
- Calcitonin gene-related peptide induces the histone H3 lysine 9 acetylation in astrocytes associated with neuroinflammation in rats with neuropathic pain.CNS neuroscience & therapeutics · 2021Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Astrocytes play a number of important physiological roles in CNS homeostasis. Inflammation stimulates astrocytes to secrete cytokines and chemokines that guide macrophages/microglia and T cells to sites of injury/inflammation. Herein, we describe how these processes are controlled by the suppressor of cytokine signaling (SOCS) proteins, a family of proteins that negatively regulate adaptive and innate immune responses. In this study, we describe that the immunomodulatory cytokine IFN-beta induces SOCS-1 and SOCS-3 expression in primary astrocytes at the transcriptional level. SOCS-1 and SOCS-3 transcriptional activity is induced by IFN-beta through IFN-gamma activation site (GAS) elements within their promoters. Studies in STAT-1alpha-deficient astrocytes indicate that STAT-1alpha is required for IFN-beta-induced SOCS-1 expression, while STAT-3 small interfering RNA studies demonstrate that IFN-beta-induced SOCS-3 expression relies on STAT-3 activation. Specific small interfering RNA inhibition of IFN-beta-inducible SOCS-1 and SOCS-3 in astrocytes enhances their proinflammatory responses to IFN-beta stimulation, such as heightened expression of the chemokines CCL2 (MCP-1), CCL3 (MIP-1alpha), CCL4 (MIP-1beta), CCL5 (RANTES), and CXCL10 (IP-10), and promoting chemotaxis of macrophages and CD4(+) T cells. These results indicate that IFN-beta induces SOCS-1 and SOCS-3 in primary astrocytes to attenuate its own chemokine-related inflammation in the CNS.
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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.