scholarly journals Gene expression analysis of the innate immune system during early rearing and weaning of meagre (Argyrosomus regius)

2019 ◽  
Vol 94 ◽  
pp. 819-832
Author(s):  
Cindy Campoverde ◽  
Douglas J. Milne ◽  
Christopher J. Secombes ◽  
Alicia Estévez ◽  
Enric Gisbert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Expression Analysis ◽  
Innate Immune System ◽  
Gene Expression Analysis ◽  
Innate Immune ◽  
Argyrosomus Regius ◽  
Early Rearing

scholarly journals Candidate innate immune system gene expression in the ecological model Daphnia

2011 ◽  
Vol 35 (10) ◽  
pp. 1068-1077 ◽  
Author(s):  
Ellen Decaestecker ◽  
Pierrick Labbé ◽  
Kirsten Ellegaard ◽  
Judith E. Allen ◽  
Tom J. Little
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Innate Immune System ◽  
Ecological Model ◽  
Innate Immune

Inflammation of the cystic fibrosis mouse small intestine

2004 ◽  
Vol 286 (6) ◽  
pp. G1032-G1041 ◽  
Author(s):  
Oxana Norkina ◽  
Simran Kaur ◽  
Donna Ziemer ◽  
Robert C. De Lisle
Keyword(s):  
Gene Expression ◽  
Cystic Fibrosis ◽  
Small Intestine ◽  
Immune System ◽  
Mast Cells ◽  
Innate Immune System ◽  
Innate Immune ◽  
Serum Amyloid ◽  
Mouse Small Intestine ◽  
Cytochrome P 450

The CFTR null mouse [cystic fibrosis (CF) mouse] has a severe intestinal phenotype that serves as a model for CF-related growth deficiency, meconium ileus, and distal intestinal obstructive syndrome. DNA microarray analysis was used to investigate gene expression in the CF mouse small intestine. Sixty-one genes exhibited a statistically significant twofold or greater increase in expression, and 98 genes were downregulated twofold or greater. Of the upregulated genes, most were associated with inflammation and included markers for cells of the innate immune system (mast cells and neutrophils) and for acute-phase genes (serum amyloid A and complement factors). The downregulated genes include 10 cytochrome P-450 genes; several are involved in lipid metabolism, and several are involved in various transport processes. Confirmation by quantitative RT-PCR showed gene expression was significantly increased for mast cell protease 2 (27-fold), hematopoietic cell transcript 1 (17-fold), serum amyloid A3 (2.9-fold), suppressor of cytokine signaling 3 (2.0-fold), leucine-rich α2-glycoprotein (21-fold), resistin-like molecule-β (49-fold), and Muclin (2.5-fold) and was significantly decreased for cytochrome P-450 4a10 (28-fold) and cubilin (114-fold). Immune cell infiltration was confirmed histologically by staining for mast cells and neutrophils. These data demonstrate that the CF intestine exhibits an inflammatory state with upregulation of components of the innate immune system.

scholarly journals Digital gene expression analysis of NSCLC-patients reveals strong immune pressure, resulting in an immune escape under immunotherapy

BMC Cancer ◽  
2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Michael Wessolly ◽  
Susann Stephan-Falkenau ◽  
Anna Streubel ◽  
Marcel Wiesweg ◽  
Sabrina Borchert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Expression Analysis ◽  
Antigen Processing ◽  
Gene Expression Analysis ◽  
Immune Escape ◽  
Gene Set Enrichment Analysis ◽  
Immune Activity ◽  
Immune Pressure ◽  
Mutational Hotspots

Abstract Background Immune checkpoint inhibitors (ICIs) are currently one of the most promising therapy options in the field of oncology. Although the first pivotal ICI trial results were published in 2011, few biomarkers exist to predict their therapy outcome. PD-L1 expression and tumor mutational burden (TMB) were proven to be sometimes-unreliable biomarkers. We have previously suggested the analysis of processing escapes, a qualitative measurement of epitope structure alterations under immune system pressure, to provide predictive information on ICI response. Here, we sought to further validate this approach and characterize interactions with different forms of immune pressure. Methods We identified a cohort consisting of 48 patients with advanced non-small cell lung cancer (NSCLC) treated with nivolumab as ICI monotherapy. Tumor samples were subjected to targeted amplicon-based sequencing using a panel of 22 cancer-associated genes covering 98 mutational hotspots. Altered antigen processing was predicted by NetChop, and MHC binding verified by NetMHC. The NanoString nCounter® platform was utilized to provide gene expression data of 770 immune-related genes. Patient data from 408 patients with NSCLC were retrieved from The Cancer Genome Atlas (TCGA) as a validation cohort. Results The two immune escape mechanisms of PD-L1 expression (TPS score) (n = 18) and presence of altered antigen processing (n = 10) are mutually non-exclusive and can occur in the same patient (n = 6). Both mechanisms have exclusive influence on different genes and pathways, according to differential gene expression analysis and gene set enrichment analysis, respectively. Interestingly, gene expression patterns associated with altered processing were enriched in T cell and NK cell immune activity. Though both mechanisms influence different genes, they are similarly linked to increased immune activity. Conclusion Pressure from the immune system will lay the foundations for escape mechanisms, leading to acquisition of resistance under therapy. Both PD-L1 expression and altered antigen processing are induced similarly by pronounced immunoactivity but in different context. The present data help to deepen our understanding of the underlying mechanisms behind those immune escapes.

scholarly journals Brain Death Enhances Activation of the Innate Immune System and Leads to Reduced Renal Metabolic Gene Expression

2019 ◽  
Vol 103 (9) ◽  
pp. 1821-1833 ◽  
Author(s):  
Laura J. Zitur ◽  
Peter J. Chlebeck ◽  
Scott K. Odorico ◽  
Juan S. Danobeitia ◽  
Tiffany J. Zens ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Brain Death ◽  
Innate Immune System ◽  
Innate Immune ◽  
Metabolic Gene ◽  
Metabolic Gene Expression

scholarly journals CREB pathway links PGE2 signaling with macrophage polarization

2015 ◽  
Vol 112 (51) ◽  
pp. 15642-15647 ◽  
Author(s):  
Bing Luan ◽  
Young-Sil Yoon ◽  
John Le Lay ◽  
Klaus H. Kaestner ◽  
Susan Hedrick ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Immune System ◽  
Insulin Sensitivity ◽  
Innate Immune System ◽  
Marker Gene ◽  
Innate Immune ◽  
M2 Polarization ◽  
Marker Gene Expression

Obesity is thought to promote insulin resistance in part via activation of the innate immune system. Increases in proinflammatory cytokine production by M1 macrophages inhibit insulin signaling in white adipose tissue. In contrast, M2 macrophages have been found to enhance insulin sensitivity in part by reducing adipose tissue inflammation. The paracrine hormone prostaglandin E2 (PGE2) enhances M2 polarization in part through activation of the cAMP pathway, although the underlying mechanism is unclear. Here we show that PGE2 stimulates M2 polarization via the cyclic AMP-responsive element binding (CREB)-mediated induction of Krupple-like factor 4 (KLF4). Targeted disruption of CREB or the cAMP-regulated transcriptional coactivators 2 and 3 (CRTC2/3) in macrophages down-regulated M2 marker gene expression and promoted insulin resistance in the context of high-fat diet feeding. As re-expression of KLF4 rescued M2 marker gene expression in CREB-depleted cells, our results demonstrate the importance of the CREB/CRTC pathway in maintaining insulin sensitivity in white adipose tissue via its effects on the innate immune system.

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