ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Major differences in the responses of primary human leukocyte subsets to IFN-beta.
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 45 papers, 1 of them a synthesis that pooled it.
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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- The cytokines interleukin-6 and interferon-α induce distinct microglia phenotypes.Journal of neuroinflammation · 2022Pooled it
- The ISG Atlas: a loss-of-function analysis characterizes antiviral properties of interferon stimulated genes.Nature communications · 2026Article
- High baseline CD317 expression on T cells predicts favorable anifrolumab response in systemic lupus erythematosus.Frontiers in immunology · 2026Article
- MITD1 is a brain-specific interferon-inducible factor that inhibits flavivirus replication.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Recent Advances of Type I Interferon on the Regulation of Immune Cells and the Treatment of Systemic Lupus Erythematosus.Journal of inflammation research · 2025Review
- Role of IFN-α in Rheumatoid Arthritis.Current rheumatology reports · 2024Review
- Upregulation of IFN-stimulated genes persists beyond the transitory broad immunologic changes of acute HIV-1 infection.iScience · 2023Article
- CRISPRi screens in human iPSC-derived astrocytes elucidate regulators of distinct inflammatory reactive states.Nature neuroscience · 2022Article
- Roles of Infection in Psoriasis.International journal of molecular sciences · 2022Review
- Interferon stimulated binding of ISRE is cell type specific and is predicted by homeostatic chromatin state.Cytokine: X · 2021Article
- Comparative Cell Surface Proteomic Analysis of the Primary Human T Cell and Monocyte Responses to Type I Interferon.Frontiers in immunology · 2021Article
- The influence of interferon on healthy and diseased skin.Cytokine · 2020Review
- Hypersensitive IFN Responses in Lupus Keratinocytes Reveal Key Mechanistic Determinants in Cutaneous Lupus.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Multiplexed Gene Expression as a Characterization of Bioactivity for Interferon Beta (IFN-β) Biosimilar Candidates: Impact of Innate Immune Response Modulating Impurities (IIRMIs).The AAPS journal · 2019Article
- Fine-Tuning of Type I Interferon Response by STAT3.Frontiers in immunology · 2019Review
- Responses to Cytokines and Interferons that Depend upon JAKs and STATs.Cold Spring Harbor perspectives in biology · 2018Review
- Article
- The molecular basis for differential type I interferon signaling.The Journal of biological chemistry · 2017Review
- Dendritic cell maturation, but not type I interferon exposure, restricts infection by HTLV-1, and viral transmission to T-cells.PLoS pathogens · 2017Article
- Physiological evidence for diversification of IFNα- and IFNβ-mediated response programs in different autoimmune diseases.Arthritis research & therapy · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Treatment of cell lines with type I IFNs activates the formation of IFN-stimulated gene factor 3 (STAT1/STAT2/IFN regulatory factor-9), which induces the expression of many genes. To study this response in primary cells, we treated fresh human blood with IFN-β and used flow cytometry to analyze phosphorylated STAT1, STAT3, and STAT5 in CD4(+) and CD8(+) T cells, B cells, and monocytes. The activation of STAT1 was remarkably different among these leukocyte subsets. In contrast to monocytes and CD4(+) and CD8(+) T cells, few B cells activated STAT1 in response to IFN-β, a finding that could not be explained by decreased levels of IFNAR2 or STAT1 or enhanced levels of suppressor of cytokine signaling 1 or relevant protein tyrosine phosphatases in B cells. Microarray and real-time PCR analyses revealed the induction of STAT1-dependent proapoptotic mRNAs in monocytes but not in B cells. These data show that IFN-stimulated gene factor 3 or STAT1 homodimers are not the main activators of gene expression in primary B cells of healthy humans. Notably, in B cells and, especially in CD4(+) T cells, IFN-β activated STAT5 in addition to STAT3, with biological effects often opposite from those driven by activated STAT1. These data help to explain why IFN-β increases the survival of primary human B cells and CD4(+) T cells but enhances the apoptosis of monocytes, as well as to understand how leukocyte subsets are differentially affected by endogenous type I IFNs during viral or bacterial infections and by type I IFN treatment of patients with multiple sclerosis, hepatitis, or cancer.
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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.