ArticleClinical and experimental immunology1999
Dendritic cell-derived nitric oxide is involved in IL-4-induced suppression of experimental allergic encephalomyelitis (EAE) in Lewis rats.
Article in Clinical and experimental immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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Who cites it
9 citing papers in PubMed, 34 citations in OpenAlex.
- A functional interleukin-4 homolog is encoded in the genome of infectious laryngotracheitis virus: Unveiling a novel virulence factor.PLoS pathogens · 2025Article
- The immune system of chicken and its response to H9N2 avian influenza virus.The veterinary quarterly · 2023Review
- Polyanhydride Nanoparticles Induce Low Inflammatory Dendritic Cell Activation Resulting in CD8International journal of nanomedicine · 2020Article
- The role of nitric oxide in metabolic regulation of Dendritic cell immune function.Cancer letters · 2018Review
- Nitric oxide controls an inflammatory-like Ly6C(hi)PDCA1+ DC subset that regulates Th1 immune responses.Journal of leukocyte biology · 2011Article
- Suppressive and pro-inflammatory roles for IL-4 in the pathogenesis of experimental drug-induced liver injury: a review.Expert opinion on drug metabolism & toxicology · 2010Review
- Production of nitric oxide and self-nitration of proteins during monocyte differentiation to dendritic cells.Journal of physiology and biochemistry · 2005Article
- Dendritic cells, T cell tolerance and therapy of adverse immune reactions.Clinical and experimental immunology · 2003Review
- Suppression of ongoing experimental allergic encephalomyelitis (EAE) in Lewis rats: synergistic effects of myelin basic protein (MBP) peptide 68-86 and IL-4.Clinical and experimental immunology · 2000Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytokines play a crucial role in initiating and perpetuating EAE, an animal model of multiple sclerosis (MS). A low dose of IL-4, administered by the nasal route over 5 days (100 ng/rat per day) prior to immunization, improved clinical scores of EAE induced in Lewis rats with myelin basic protein (MBP) peptide 68-86 (MBP 68-86). We examined whether dendritic cells (DC) may have contributed to the amelioration of the disease process. These professional antigen-presenting cells (APC) not only activate T cells, but also tolerize T cells to antigens, thereby minimizing autoimmune reactions. We found that IL-4 administration enhanced proliferation of DC. In comparison with DC of PBS-treated rats, DC from IL-4-treated rats secreted high levels of interferon-gamma (IFN-gamma) and IL-10. Nitric oxide (NO) production by DC was also strongly augmented in IL-4-treated rats. In vitro studies showed that IL-4 stimulated DC expansion and that IFN-gamma enhanced NO production by DC. DC-derived NO promoted apoptosis of autoreactive T cells. These results indicate that nasal administration of IL-4 promotes activation of DC and induces production of IFN-gamma and IL-10 by DC. IL-10 suppresses antigen presentation by DC, while IFN-gamma induces NO production by DC which leads to apoptosis in autoreactive T cells. Such a DC-derived negative feedback loop might contribute to the clinical improvement observed in EAE.
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