Downregulation of exosomal MHC-I promotes glioma cells escaping from systemic immunosurveillance

Sun, Ting; Li, Yanyan; Wu, Jie; Cao, Yufei; Yang, Ying; He, Yue; Huang, Wei; Liu, Bin; Yang, Wei

doi:10.1016/j.nano.2022.102605

Cited by 9 publications

(7 citation statements)

References 32 publications

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“…As evidence for the importance of MHC expression, upregulating glioma-derived exosomal MHC-I expression can assist CD8+ T cells in recognizing tumour cells, interrupting glioma cells from evading immunosurveillance. 197 Cooperatively, a large scale of stochastic mutation induced by TMZ 29 , 98 will accelerate this selection progression to promote surface immunogenic MHC-antigen complex loss. Thus, clonal evolution, 98 subtype switching, 198 and LOH in MHC and B2M genes 199 after treatment potentially alter the GBM antigen repertoire longitudinally, resulting in antigen loss for vaccine therapy.…”

Section: Challenges For the Gbm Vaccinementioning

confidence: 99%

Glioblastoma vaccines: past, present, and opportunities

Xiong,

Raphael,

Olin

et al. 2024

eBioMedicine

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Section: Challenges For the Gbm Vaccinementioning

confidence: 99%

Glioblastoma vaccines: past, present, and opportunities

Xiong,

Raphael,

Olin

et al. 2024

eBioMedicine

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“…This question may be attributed to the regulation of exosomes on the immune system. Some tumor-derived exosomes downregulate surface major histocompatibility complex I (MHC-I) levels, leading to CD8 + T cell dysfunction [ 37 ]. Similarly, certain tumor-derived exosomes carry increased programmed death ligand 1 (PD-L1) on their surface, which is an inhibitory checkpoint molecule hindering the function of cytotoxic T cells and macrophages [ 38 ].…”

Section: Hbv Utilizes the Release And Transport Of Exosomesmentioning

confidence: 99%

Exosomes target HBV-host interactions to remodel the hepatic immune microenvironment

Wu,

Niu,

Shi

2024

J Nanobiotechnol

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Chronic hepatitis B poses a significant global burden, modulating immune cells, leading to chronic inflammation and long-term damage. Due to its hepatotropism, the hepatitis B virus (HBV) cannot infect other cells. The mechanisms underlying the intercellular communication among different liver cells in HBV-infected individuals and the immune microenvironment imbalance remain elusive. Exosomes, as important intercellular communication and cargo transportation tools between HBV-infected hepatocytes and immune cells, have been shown to assist in HBV cargo transportation and regulate the immune microenvironment. However, the role of exosomes in hepatitis B has only gradually received attention in recent years. Minimal literature has systematically elaborated on the role of exosomes in reshaping the immune microenvironment of the liver. This review unfolds sequentially based on the biological processes of exosomes: exosomes’ biogenesis, release, transport, uptake by recipient cells, and their impact on recipient cells. We delineate how HBV influences the biogenesis of exosomes, utilizing exosomal covert transmission, and reshapes the hepatic immune microenvironment. And based on the characteristics and functions of exosomes, potential applications of exosomes in hepatitis B are summarized and predicted. Graphical Abstract

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“…There is a growing interest in the role of exosomes, including exosome-containing MHC-1, in the priming of CD8 + T cells, predominantly investigated in tumor cell-derived exosomes [213]. Several factors regulate MHC-1 levels in exosomes, including HDAC and NF-kB signaling [214].…”

Section: Future Research Directionsmentioning

confidence: 99%

Redefining Autoimmune Disorders’ Pathoetiology: Implications for Mood and Psychotic Disorders’ Association with Neurodegenerative and Classical Autoimmune Disorders

Anderson¹,

Almulla

Reíter

et al. 2023

Cells

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Although previously restricted to a limited number of medical conditions, there is a growing appreciation that ‘autoimmune’ (or immune-mediated) processes are important aspects of a wide array of diverse medical conditions, including cancers, neurodegenerative diseases and psychiatric disorders. All of these classes of medical conditions are associated with alterations in mitochondrial function across an array of diverse cell types. Accumulating data indicate the presence of the mitochondrial melatonergic pathway in possibly all body cells, with important consequences for pathways crucial in driving CD8+ T cell and B-cell ‘autoimmune’-linked processes. Melatonin suppression coupled with the upregulation of oxidative stress suppress PTEN-induced kinase 1 (PINK1)/parkin-driven mitophagy, raising the levels of the major histocompatibility complex (MHC)-1, which underpins the chemoattraction of CD8+ T cells and the activation of antibody-producing B-cells. Many factors and processes closely associated with autoimmunity, including gut microbiome/permeability, circadian rhythms, aging, the aryl hydrocarbon receptor, brain-derived neurotrophic factor (BDNF) and its receptor tyrosine receptor kinase B (TrkB) all interact with the mitochondrial melatonergic pathway. A number of future research directions and novel treatment implications are indicated for this wide collection of poorly conceptualized and treated medical presentations. It is proposed that the etiology of many ‘autoimmune’/‘immune-mediated’ disorders should be conceptualized as significantly determined by mitochondrial dysregulation, with alterations in the mitochondrial melatonergic pathway being an important aspect of these pathoetiologies.

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Downregulation of exosomal MHC-I promotes glioma cells escaping from systemic immunosurveillance

Cited by 9 publications

References 32 publications

Glioblastoma vaccines: past, present, and opportunities

Glioblastoma vaccines: past, present, and opportunities

Exosomes target HBV-host interactions to remodel the hepatic immune microenvironment

Redefining Autoimmune Disorders’ Pathoetiology: Implications for Mood and Psychotic Disorders’ Association with Neurodegenerative and Classical Autoimmune Disorders

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