ArticleNature communications2021
Early-life-trauma triggers interferon-β resistance and neurodegeneration in a multiple sclerosis model via downregulated β1-adrenergic signaling.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06718920 (Single-center Observational Study to Characterize Adverse Childhood Experiences), which is not on this map. Cited by 8 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.
Single-center Observational Study to Characterize Adverse Childhood Experiences (ACE) in Patients With Multiple Sclerosis and Their Impact on Quality of Life, Disease Coping Strategies, and Adherence to Disease Course-modifying Therapies
Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- β-Adrenergic receptors as immunomodulators in T cells: mechanisms of neuroimmune crosstalk and pathophysiological implications.Molecular medicine (Cambridge, Mass.) · 2026Review
- Decreased lymph node estrogen levels cause nonremitting progressive experimental autoimmune encephalomyelitis disease.PNAS nexus · 2025Article
- Cathepsin K deficiency prevented stress-related thrombosis in a mouse FeClCellular and molecular life sciences : CMLS · 2024Article
- Adverse Childhood Experiences and the Risk of Multiple Sclerosis Development: A Review of Potential Mechanisms.International journal of molecular sciences · 2024Review
- Similar neural pathways link psychological stress and brain-age in health and multiple sclerosis.iScience · 2023Article
- Estrogen receptor alpha signaling in dendritic cells modulates autoimmune disease phenotype in mice.EMBO reports · 2023Article
- Association of adverse childhood experiences with the development of multiple sclerosis.Journal of neurology, neurosurgery, and psychiatry · 2022Article
- Role of adrenergic receptor signalling in neuroimmune communication.Current research in immunology · 2021Review
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
No grant is acknowledged in the PubMed record.
Abstract
Environmental triggers have important functions in multiple sclerosis (MS) susceptibility, phenotype, and trajectory. Exposure to early life trauma (ELT) has been associated with higher relapse rates in MS patients; however, the underlying mechanisms are not well-defined. Here we show ELT induces mechanistic and phenotypical alterations during experimental autoimmune encephalitis (EAE). ELT sustains downregulation of immune cell adrenergic receptors, which can be attributed to chronic norepinephrine circulation. ELT-subjected mice exhibit interferon-β resistance and neurodegeneration driven by lymphotoxin and CXCR2 involvement. These phenotypic changes are observed in control EAE mice treated with β1 adrenergic receptor antagonist. Conversely, β1 adrenergic receptor agonist treatment to ELT mice abrogates phenotype changes via restoration of immune cell β1 adrenergic receptor function. Our results indicate that ELT alters EAE phenotype via downregulation of β1 adrenergic signaling in immune cells. These results have implications for the effect of environmental factors in provoking disease heterogeneity and might enable prediction of long-term outcomes in MS.
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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.