Enhanced expression of MHC class I molecules on cultured human thyroid follicular cells infected with reovirus through induction of type 1 interferons

Atta, Mustafa S.; Irving, Will; Powell, R J; Todd, Ian

doi:10.1111/j.1365-2249.1995.tb02287.x

Cited by 18 publications

(6 citation statements)

References 30 publications

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“…IFNα mediates a long-lasting and preferential MHC class I overexpression in non-immune cells, such as human pancreatic beta cells and thyroid follicular cells, which usually lack MHC class 1 expression. This finding suggests that IFNα might amplify antigen presentation in type 1 diabetes and Hashimoto thyroiditis 133,134 . The increased expression of MHC class I molecules on skeletal muscle cells of patients with IIM probably leads to increased susceptibility of the cells to cytotoxic T cell attack and endoplasmic reticular (ER) stress–mediated cell death 135,136 .…”

Section: Immune-mediated Disease Mechanismsmentioning

confidence: 84%

Risk factors and disease mechanisms in myositis

et al. 2018

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Autoimmune diseases develop as a result of chronic inflammation owing to interactions between genes and the environment. However, the mechanisms by which autoimmune diseases evolve remain poorly understood. Newly discovered risk factors and pathogenic processes in the various idiopathic inflammatory myopathy (IIM) phenotypes (known collectively as myositis) have illuminated innovative approaches for understanding these diseases. The HLA 8.1 ancestral haplotype is a key risk factor for major IIM phenotypes in some populations, and several genetic variants associated with other autoimmune diseases have been identified as IIM risk factors. Environmental risk factors are less well studied than genetic factors but might include viruses, bacteria, ultraviolet radiation, smoking, occupational and perinatal exposures and a growing list of drugs (including biologic agents) and dietary supplements. Disease mechanisms vary by phenotype, with evidence of shared innate and adaptive immune and metabolic pathways in some phenotypes but unique pathways in others. The heterogeneity and rarity of the IIMs make advancements in diagnosis and treatment cumbersome. Novel approaches, better-defined phenotypes, and international, multidisciplinary consensus have contributed to progress, and it is hoped that these methods will eventually enable therapeutic intervention before the onset or major progression of disease. In the future, preemptive strategies for IIM management might be possible.

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Section: Immune-mediated Disease Mechanismsmentioning

confidence: 84%

Risk factors and disease mechanisms in myositis

et al. 2018

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“…Stroke, on the other hand, is not well recognized as a potential adverse event, being limited to a few case reports. 19 , 20 Nonetheless, it is biologically plausible that this event is associated with IFN-β because this drug may alter wall competence or enhance the major histocompatibility complex-1 molecule expression of platelets and other cells, 21 , 22 resulting in enhanced platelet adhesion to the endothelium. 22 , 23 Furthermore, it has been reported that IFN-β may exacerbate other underlying autoimmune diseases (such as vasculitis).…”

Section: Discussionmentioning

confidence: 99%

Evaluating the safety of β-interferons in MS

et al. 2017

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Objective:To examine the association between interferon-β (IFN-β) and potential adverse events using population-based health administrative data in British Columbia, Canada.Methods:Patients with relapsing-remitting multiple sclerosis (RRMS) who were registered at a British Columbia Multiple Sclerosis Clinic (1995–2004) were eligible for inclusion and were followed up until death, absence from British Columbia, exposure to a non–IFN-β disease-modifying drug, or December 31, 2008. Incidence rates were estimated for each potential adverse event (selected a priori and defined with ICD-9/10 diagnosis codes from physician and hospital claims). A nested case-control study was conducted to assess the odds of previous IFN-β exposure for each potential adverse event with at least 30 cases. Cases were matched by age (±5 years), sex, and year of cohort entry, with up to 20 randomly selected (by incidence density sampling) controls. Odds ratios (ORs) with 95% confidence intervals (95% CIs) were estimated with conditional logistic regression adjusted for age at cohort entry.Results:Of the 2,485 eligible patients, 77.9% were women, and 1,031 were treated with IFN-β during follow-up. From the incidence analyses, 27 of the 47 potential adverse events had at least 30 cases. Patients with incident stroke (ORadj 1.83, 95% CI 1.16–2.89), migraine (ORadj 1.55, 95% CI 1.18–2.04), depression (ORadj 1.33, 95% CI 1.13–1.56), and hematologic abnormalities (ORadj 1.32, 95% CI 1.01–1.72) were more likely to have previous exposure to IFN-β than controls.Conclusions:Among patients with RRMS, IFN-β was associated with a 1.8- and 1.6-fold increase in the risk of stroke and migraine and 1.3-fold increases in depression and hematologic abnormalities.

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“…response (Atta et al, 1995). GSCs express low levels of MHC-I, presumably as a mechanism for evading immune surveillance (Wu et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…TMZ was shown to induce MHC-I mRNA and protein expression in GSCs. MHC-I proteins are polymorphic and display cellular peptides as cell surface antigens to activate an immune response (Atta et al, 1995). GSCs express low levels of MHC-I, presumably as a mechanism for evading immune surveillance (Wu et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Temozolomide increases MHC‐I expression via NF‐κB signaling in glioma stem cells

Zhang

Qiu

Guan

et al. 2017

Cell Biology International

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Gliomas are the most common and primary tumors of the central nervous system in adults. Temozolomide (TMZ) is the main drug used to treat glioma; however, prognosis remains poor for most patients. Glioma stem cells (GSCs) are thought to enable glioma initiation and evasion from immune surveillance; their immunogenicity can be determined by expression of major histocompatibility complex (MHC)-I. The present study investigated the effect of TMZ on MHC-I expression in GSCs. Glioma spheres were cultured in serum-free medium containing epidermal growth factor, basic fibroblast growth factor, and B27; MHC-I expression was detected by immunocytochemistry, quantitative real-time PCR, and flow cytometry. Nuclear factor (NF)-κB expression in glioma stem cells was detected by Western blot. TMZ enhanced MHC-I expression in GSCs, and NF-κB was activated. TMZ treatment increased MHC-I expression via modulation of NF-κB signaling in GSCs. In addition to being a chemotherapeutic agent, TMZ may also serve as an immunomodulatory agent in the treatment of glioma patients.

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Enhanced expression of MHC class I molecules on cultured human thyroid follicular cells infected with reovirus through induction of type 1 interferons

Cited by 18 publications

References 30 publications

Risk factors and disease mechanisms in myositis

Risk factors and disease mechanisms in myositis

Evaluating the safety of β-interferons in MS

Temozolomide increases MHC‐I expression via NF‐κB signaling in glioma stem cells

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