scholarly journals Innate Immune CD11b+Gr-1+Cells, Suppressor Cells, Affect the Immune Response during Theiler’s Virus-Induced Demyelinating Disease

2009 ◽  
Vol 183 (11) ◽  
pp. 6971-6980 ◽  
Author(s):  
Jenna L. Bowen ◽  
Julie K. Olson
Keyword(s):  
Immune Response ◽  
Demyelinating Disease ◽  
Suppressor Cells ◽  
Innate Immune ◽  
Theiler's Virus

scholarly journals A multiscale signalling network map of innate immune response in cancer reveals cell heterogeneity signatures

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Maria Kondratova ◽  
Urszula Czerwinska ◽  
Nicolas Sompairac ◽  
Sebastian D. Amigorena ◽  
Vassili Soumelis ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Molecular Mechanisms ◽  
Chemical Species ◽  
Suppressor Cells ◽  
Tumour Microenvironment ◽  
Innate Immune ◽  
Literature Mining ◽  
Cell Type ◽  
Signalling Network

Abstract The lack of integrated resources depicting the complexity of the innate immune response in cancer represents a bottleneck for high-throughput data interpretation. To address this challenge, we perform a systematic manual literature mining of molecular mechanisms governing the innate immune response in cancer and represent it as a signalling network map. The cell-type specific signalling maps of macrophages, dendritic cells, myeloid-derived suppressor cells and natural killers are constructed and integrated into a comprehensive meta map of the innate immune response in cancer. The meta-map contains 1466 chemical species as nodes connected by 1084 biochemical reactions, and it is supported by information from 820 articles. The resource helps to interpret single cell RNA-Seq data from macrophages and natural killer cells in metastatic melanoma that reveal different anti- or pro-tumor sub-populations within each cell type. Here, we report a new open source analytic platform that supports data visualisation and interpretation of tumour microenvironment activity in cancer.

scholarly journals Differential expression of multiple kallikreins in a viral model of multiple sclerosis points to unique roles in the innate and adaptive immune response

2014 ◽  
Vol 395 (9) ◽  
pp. 1063-1073 ◽  
Author(s):  
Michael Panos ◽  
George P. Christophi ◽  
Moses Rodriguez ◽  
Isobel A. Scarisbrick
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Immune Response ◽  
Demyelinating Disease ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Axon Degeneration ◽  
Functional Link ◽  
The Brain

Abstract Recent studies provide a functional link between kallikrein 6 (Klk6) and the development and progression of disease in patients with multiple sclerosis (MS) and in its murine models. To evaluate the involvement of additional kallikrein family members, we compared Klk6 expression with four other kallikreins (Klk1, Klk7, Klk8, and Klk10) in the brain and spinal cord of mice infected with Theiler’s murine encephalomyelitis virus, an experimental model of progressive MS. The robust upregulation of Klk6 and Klk8 in the brain during the acute phase of viral encephalitis and in the spinal cord during disease development and progression points to their participation in inflammation, demyelination, and progressive axon degeneration. More limited changes in Klk1, Klk7, and Klk10 were also observed. In addition, Klk1, Klk6, and Klk10 were dynamically regulated in T cells in vitro as a recall response to viral antigen and in activated monocytes, pointing to their activities in the development of adaptive and innate immune function. Together, these results point to overlapping and unique roles for multiple kallikreins in the development and progression of virus-mediated central nervous system inflammatory demyelinating disease, including activities in the development of the adaptive and innate immune response, in demyelination, and in progressive axon degeneration.

scholarly journals Innate Immune Responses and Viral-Induced Neurologic Disease

2018 ◽  
Vol 8 (1) ◽  
pp. 3 ◽  
Author(s):  
Yuting Cheng ◽  
Dominic Skinner ◽  
Thomas Lane
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Demyelinating Disease ◽  
Association Studies ◽  
Adaptive Immune Response ◽  
Neutrophil Infiltration ◽  
Innate Immune ◽  
Clinical Relapse ◽  
Genome Wide Association Studies ◽  
Neurologic Disease

Multiple sclerosis (MS) is a disease of the central nervous system (CNS) characterized by chronic neuroinflammation, axonal damage, and demyelination. Cellular components of the adaptive immune response are viewed as important in initiating formation of demyelinating lesions in MS patients. This notion is supported by preclinical animal models, genome-wide association studies (GWAS), as well as approved disease modifying therapies (DMTs) that suppress clinical relapse and are designed to impede infiltration of activated lymphocytes into the CNS. Nonetheless, emerging evidence demonstrates that the innate immune response e.g., neutrophils can amplify white matter damage through a variety of different mechanisms. Indeed, using a model of coronavirus-induced neurologic disease, we have demonstrated that sustained neutrophil infiltration into the CNS of infected animals correlates with increased demyelination. This brief review highlights recent evidence arguing that targeting the innate immune response may offer new therapeutic avenues for treatment of demyelinating disease including MS.

scholarly journals Exosomes Secreted by Microglia During Virus Infection in the Central Nervous System Activate an Inflammatory Response in Bystander Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Nhungoc Luong ◽  
Julie K. Olson
Keyword(s):  
Central Nervous System ◽  
Immune Response ◽  
Nervous System ◽  
Demyelinating Disease ◽  
Innate Immune ◽  
Viral Rna ◽  
Type I Interferons ◽  
Type I ◽  
The Central Nervous System ◽  
Bystander Cells

Microglia become persistently infected during Theiler’s murine encephalomyelitis virus (TMEV) infection in the central nervous system (CNS) of susceptible mice. We have previously shown that microglia infected with TMEV become activated through the innate immune receptors to express type I interferons, cytokines, and chemokines. Persistent TMEV infection in the CNS promotes chronic neuroinflammation and development of demyelinating disease similar to multiple sclerosis. In the current studies, we wanted to determine whether TMEV-infected microglia secrete exosomes which contribute to neuroinflammation in the CNS thus promoting the development of demyelinating disease. Exosomes are vesicles containing RNA, DNA, and proteins that are released from one cell and taken up by another cell to facilitate communication between cells. These studies isolated exosomes secreted by microglia during TMEV infection in vitro as well as exosomes secreted by microglia during early TMEV infection in mice. These studies show that microglia secrete exosomes during TMEV infection which contain the viral RNA coding region. The exosomes secreted by microglia during TMEV infection can be taken up by uninfected bystander cells, including CNS resident microglia, astrocytes, and neurons. The viral RNA in the exosomes can be transferred to the bystander cells. In addition, the bystander cells that took up these exosomes were activated through the innate immune response to express type I interferons, IFNα and IFNβ, pro-inflammatory cytokines, IL-6, IL-12, and TNFα, and chemokines, CCL2. Most interestingly, exosomes secreted by microglia during early TMEV infection in mice activated an inflammatory response when transferred to the brains of naïve mice. These results show that exosomes secreted by microglia during early TMEV infection contain viral RNA and can activate uninfected bystander CNS cells to promote an inflammatory immune response. Thus, exosomes secreted by microglia during virus infection may promote viral persistence and neuroinflammation which contributes to the development of demyelinating disease.

Oral Immune Activation by Disgust and Disease-Related Pictures

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Negative Control ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Immune Markers ◽  
Before And After ◽  
Secondary Analyses ◽  
Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

Sign in / Sign up

Export Citation Format

Share Document