ArticleProceedings of the National Academy of Sciences of the United States of America2011
The role of cell type-specific responses in IFN-β therapy of multiple sclerosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 46 citations in OpenAlex.
- Transcription factors in the development and treatment of immune disorders.Transcription · 2025Review
- Autoimmune demyelination alters hypothalamic transcriptome and endocrine function.Journal of neuroinflammation · 2024Article
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- Altered Immune Phenotypes andFrontiers in immunology · 2021Article
- Variants of genes encoding TNF receptors and ligands and proteins regulating TNF activation in familial multiple sclerosis.CNS neuroscience & therapeutics · 2020Article
- Molecular Effects of FDA-Approved Multiple Sclerosis Drugs on Glial Cells and Neurons of the Central Nervous System.International journal of molecular sciences · 2020Review
- Antiviral, Immunomodulatory and Antiproliferative Activities of Recombinant Soluble IFNAR2 without IFN-ß Mediation.Journal of clinical medicine · 2020Article
- Type I Interferon (IFN)-Regulated Activation of Canonical and Non-Canonical Signaling Pathways.Frontiers in immunology · 2020Review
- 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
- Impairment of human neural crest cell migration by prolonged exposure to interferon-beta.Archives of toxicology · 2017Article
- A novel technique to determine the cell type specific response within an in vitro co-culture model via multi-colour flow cytometry.Scientific reports · 2017Article
- Article
- Article
- Clinical perspectives of TRAIL: insights into central nervous system disorders.Cellular and molecular life sciences : CMLS · 2016Review
- TRAIL and TRAIL receptors splice variants during long-term interferon β treatment of patients with multiple sclerosis: evaluation as biomarkers for therapeutic response.Journal of neurology, neurosurgery, and psychiatry · 2016Article
- The role of a non-canonical JAK-STAT pathway in IFN therapy of poxvirus infection and multiple sclerosis: An example of Occam's Broom?JAK-STAT · 2013Review
- Candidate gene study of TRAIL and TRAIL receptors: association with response to interferon beta therapy in multiple sclerosis patients.PloS one · 2013Article
- Baseline gene expression signatures in monocytes from multiple sclerosis patients treated with interferon-beta.PloS one · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism of IFN-β therapy in relapsing-remitting multiple sclerosis (RRMS) is not well understood, but induction of apoptosis in specific leukocyte subsets is likely to be important. Enhanced expression of TNFSF10 or TNF-related apoptosis-inducing ligand (TRAIL) mRNA in unseparated leukocytes has been put forward as a therapeutic response marker, but it is unclear which leukocyte subsets express TRAIL. We investigated the basis of TRAIL expression in response to IFN-β by studying activation of STATs 1, 3, and 5, p38 MAPK, and NF-κB in different leukocyte subsets of patients with RRMS. Monocytes, B cells, and T cells showed substantial differences in the activation of p38 and the STATs in response to i.m. injection of IFN-β1a or stimulation in vitro. Induction of cell-surface TRAIL, analyzed in nine leukocyte subsets, was observed only on monocytes and granulocytes and correlated with the activation of p38 and/or NF-κB in these subsets only, in agreement with previous work in fibroblasts showing that the induction of TRAIL in response to IFN-β depends on the activation of p38 and NF-κB as well as STATs 1 and 2. We propose that, in myeloid cells, the differential activation of p38 and NF-κB and induction of TRAIL, which sensitizes cells to apoptosis, can help to explain differences in responsiveness to IFN-β therapy among patients with RRMS and, furthermore, that such differential patterns of activation and expression may also be important in understanding the therapeutic responses to IFN-α/β in hepatitis and cancer.
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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.