scholarly journals Upregulated inducible co-stimulator (ICOS) and ICOS-ligand in inclusion body myositis muscle: significance for CD8+ T cell cytotoxicity

Brain ◽  
2004 ◽  
Vol 127 (5) ◽  
pp. 1182-1190 ◽  
Author(s):  
J. Schmidt
2012 ◽  
Vol 189 (7) ◽  
pp. 3521-3527 ◽  
Author(s):  
Hee Chul Lee ◽  
Assefa Wondimu ◽  
Yihui Liu ◽  
Jennifer S. Y. Ma ◽  
Saša Radoja ◽  
...  

2020 ◽  
Vol 487 ◽  
pp. 112899
Author(s):  
Verónica Olivo Pimentel ◽  
Ala Yaromina ◽  
Damiënne Marcus ◽  
Ludwig J. Dubois ◽  
Philippe Lambin

2016 ◽  
Vol 215 (3) ◽  
pp. 387-395 ◽  
Author(s):  
Ludmila Rodrigues Pinto Ferreira ◽  
Frederico Moraes Ferreira ◽  
Helder Imoto Nakaya ◽  
Xutao Deng ◽  
Darlan da Silva Cândido ◽  
...  

AbstractChagas disease, caused by the protozoan parasite Trypanosoma cruzi, affects 7 million people in Latin American areas of endemicity. About 30% of infected patients will develop chronic Chagas cardiomyopathy (CCC), an inflammatory cardiomyopathy characterized by hypertrophy, fibrosis, and myocarditis. Further studies are necessary to understand the molecular mechanisms of disease progression. Transcriptome analysis has been increasingly used to identify molecular changes associated with disease outcomes. We thus assessed the whole-blood transcriptome of patients with Chagas disease. Microarray analysis was performed on blood samples from 150 subjects, of whom 30 were uninfected control patients and 120 had Chagas disease (1 group had asymptomatic disease, and 2 groups had CCC with either a preserved or reduced left ventricular ejection fraction [LVEF]). Each Chagas disease group displayed distinct gene expression and functional pathway profiles. The most different expression patterns were between CCC groups with a preserved or reduced LVEF. A more stringent analysis indicated that 27 differentially expressed genes, particularly those related to natural killer (NK)/CD8+ T-cell cytotoxicity, separated the 2 groups. NK/CD8+ T-cell cytotoxicity could play a role in determining Chagas disease progression. Understanding genes associated with disease may lead to improved insight into CCC pathogenesis and the identification of prognostic factors for CCC progression.


2011 ◽  
Vol 187 (8) ◽  
pp. 4119-4128 ◽  
Author(s):  
Raphael Schneider ◽  
Alma Nazlie Mohebiany ◽  
Igal Ifergan ◽  
Diane Beauseigle ◽  
Pierre Duquette ◽  
...  

Vaccine ◽  
2012 ◽  
Vol 30 (14) ◽  
pp. 2440-2447 ◽  
Author(s):  
Ying Zhou ◽  
Hui Zhang ◽  
Xin-Juan Sun ◽  
Dan Zheng ◽  
Yue-Jin Liang ◽  
...  

Brain ◽  
2019 ◽  
Vol 142 (9) ◽  
pp. 2590-2604 ◽  
Author(s):  
Steven A Greenberg ◽  
Jack L Pinkus ◽  
Sek Won Kong ◽  
Clare Baecher-Allan ◽  
Anthony A Amato ◽  
...  

Abstract Inclusion body myositis is a late onset treatment-refractory autoimmune disease of skeletal muscle associated with a blood autoantibody (anti-cN1A), an HLA autoimmune haplotype, and muscle pathology characterized by cytotoxic CD8+ T cell destruction of myofibres. Here, we report on translational studies of inclusion body myositis patient muscle compared with a diverse set of other muscle disease samples. Using available microarray data on 411 muscle samples from patients with inclusion body myositis (n = 40), other muscle diseases (n = 265), and without neuromuscular disease (normal, n = 106), we identified a signature of T-cell cytotoxicity in inclusion body myositis muscle coupled with a signature of highly differentiated CD8 T-cell effector memory and terminally differentiated effector cells. Further, we examined killer cell lectin-like receptor G1 (KLRG1) as a marker of this population of cells, demonstrated the correlation of KLRG1 gene expression with lymphocyte cytotoxicity across 28 870 human tissue samples, and identified the presence of KLRG1 on pathogenic inclusion body myositis muscle invading T cells and an increase in KLRG1 expressing T cells in inclusion body myositis blood. We examined inclusion body myositis muscle T-cell proliferation by Ki67 immunohistochemistry demonstrating that diseased muscle-invading T cells are minimally or non-proliferative, in accordance with known properties of highly differentiated or terminally differentiated T cells. We found low expression of KLRG1 on infection-protective human lymphoid tissue central memory T cells and autoimmune-protective human blood regulatory T cells. Targeting highly differentiated cytotoxic T cells could be a favourable approach to treatment of inclusion body myositis.


2014 ◽  
Vol 194 (3) ◽  
pp. 1069-1079 ◽  
Author(s):  
Evelyn Hartung ◽  
Martina Becker ◽  
Annabell Bachem ◽  
Nele Reeg ◽  
Anika Jäkel ◽  
...  

2012 ◽  
Vol 43 (1) ◽  
pp. 194-208 ◽  
Author(s):  
Orietta D'Orlando ◽  
Fang Zhao ◽  
Brigitte Kasper ◽  
Zane Orinska ◽  
Jürgen Müller ◽  
...  

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