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https://www.readbyqxmd.com/read/27933491/nlrp3-is-required-for-complement-mediated-caspase-1-and-il-1beta-activation-in-ich-short-title-for-running-head-nlrp3-is-required-for-ich
#1
Sheng-Tao Yao, Fang Cao, Jia-Lin Chen, Wei Chen, Rui-Ming Fan, Gang Li, You-Chao Zeng, Song Jiao, Xiang-Ping Xia, Chong Han, Qi-Shan Ran
Complement-mediated inflammation plays a vital role in intracerebral hemorrhage (ICH), implicating pro-inflammatory factor interleukin-1beta (IL-1β) secretion. Brain samples and contralateral hemiencephalon were all collected and detected by Western blot. NLRP3 expression was located by dual immunofluorescence staining at 1, 3, and 5 days post-ICH. Brain water content was examined post-ICH. The neural deficit scores were evaluated by observers blindly. ILs were detected by ELISA. SiRNAs targeting NLRP3 (siNLRP3), siASC, and siControl were injected to inhibit NLRP3 function...
December 8, 2016: Journal of Molecular Neuroscience: MN
https://www.readbyqxmd.com/read/27920091/interferon-gamma-limits-diabetogenic-cd8-t-cell-effector-responses-in-type-1-diabetes
#2
John P Driver, Jeremy J Racine, Cheng Ye, Deanna J Lamont, Brittney N Newby, Caroline G McPhee-Leeth, Harold D Chapman, Todd M Brusko, Yi-Guang Chen, Clayton E Mathews, David V Serreze
Type 1 diabetes development in the NOD mouse model is widely reported to be dependent on high-level production by autoreactive CD4(+) and CD8(+) T-cells of IFNγ, generally considered a pro-inflammatory cytokine. However, IFNγ can also participate in tolerance induction pathways, indicating it is not solely pro-inflammatory. This study addresses how IFNγ can suppress activation of diabetogenic CD8(+) T-cells. CD8(+) T-cells transgenically expressing the diabetogenic AI4 T-cell receptor (TCR) adoptively transferred disease to otherwise unmanipulated NOD...
December 5, 2016: Diabetes
https://www.readbyqxmd.com/read/27913646/critical-differences-between-induced-and-spontaneous-mouse-models-of-graves-disease-with-implications-for-antigen-specific-immunotherapy-in-humans
#3
Basil Rapoport, Bianca Banuelos, Holly A Aliesky, Nicole Hartwig Trier, Sandra M McLachlan
Graves' hyperthyroidism, a common autoimmune disease caused by pathogenic autoantibodies to the thyrotropin (TSH) receptor (TSHR), can be treated but not cured. This single autoantigenic target makes Graves' disease a prime candidate for Ag-specific immunotherapy. Previously, in an induced mouse model, injecting TSHR A-subunit protein attenuated hyperthyroidism by diverting pathogenic TSHR Abs to a nonfunctional variety. In this study, we explored the possibility of a similar diversion in a mouse model that spontaneously develops pathogenic TSHR autoantibodies, NOD...
December 15, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/27889607/leptin-ob-r-signaling-is-elevated-in-mice-with-sj%C3%A3-gren-s-syndrome-and-is-implicated-in-disease-pathogenesis
#4
Ting Xu, Wen Xie, Yingchun Ma, Shiliang Zhou, Lu Zhang, Jinyun Chen, Mingyuan Cai, Rurong Sun, Peirong Zhang, Shaobo Yu, Zheng Xu, Wanlan Jiang, Min Wu
Sjögren's syndrome (SjS) is a systemic autoimmune disease resulting in a severe dry mouth and dry eyes. Currently, care for patients with SjS is palliative, as no established therapeutics target the disease directly, and its pathogenetic mechanisms are uncertain. Leptin activates B cells to induce the secretion of proinflammatory and anti-inflammatory cytokines and is elevated in several autoimmune diseases. In this study, we found the expression of leptin and its receptor OB-R in mouse models of SjS are elevated both locally and systemically during SjS progression...
November 23, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27889463/noncanonical-fungal-autophagy-inhibits-inflammation-in-response-to-ifn-%C3%AE-via-dapk1
#5
Vasilis Oikonomou, Silvia Moretti, Giorgia Renga, Claudia Galosi, Monica Borghi, Marilena Pariano, Matteo Puccetti, Carlo A Palmerini, Lucia Amico, Alessandra Carotti, Lucia Prezioso, Angelica Spolzino, Andrea Finocchi, Paolo Rossi, Andrea Velardi, Franco Aversa, Valerio Napolioni, Luigina Romani
Defects in a form of noncanonical autophagy, known as LC3-associated phagocytosis (LAP), lead to increased inflammatory pathology during fungal infection. Although LAP contributes to fungal degradation, the molecular mechanisms underlying LAP-mediated modulation of inflammation are unknown. We describe a mechanism by which inflammation is regulated during LAP through the death-associated protein kinase 1 (DAPK1). The ATF6/C/EBP-β/DAPK1 axis activated by IFN-γ not only mediates LAP to Aspergillus fumigatus but also concomitantly inhibits Nod-like receptor protein 3 (NLRP3) activation and restrains pathogenic inflammation...
November 16, 2016: Cell Host & Microbe
https://www.readbyqxmd.com/read/27885834/presence-of-an-immune-system-increases-anti-tumor-effect-of-ag-nanoparticle-treated-mice
#6
Bella B Manshian, Julio Jimenez, Uwe Himmelreich, Stefaan J Soenen
To date, most nanomedical studies rely on the use of immune-deficient mice in which the contribution of the immune system on the applied therapy is ignored. Here, the degradation of silver nanoparticles (Ag NPs) is exploited as a means to treat subcutaneous tumor models in mice. To investigate the impact of the immune system, the same tumor cell type (KLN 205 murine squamous cell carcinoma) is used in a xenograft model in NOD SCIDγ immune-deficient mice and as a syngeneic model in immune-competent DBA/2 mice...
November 25, 2016: Advanced Healthcare Materials
https://www.readbyqxmd.com/read/27882092/the-influence-of-exendin-4-intervention-on-obese-diabetic-mouse-blood-and-the-pancreatic-tissue-immune-microenvironment
#7
Jinshui He, Chaowei Lian, Yanling Fang, Jinzhi Wu, Huowang Zhou, Xiaoling Ye
The aim of the study was to determine the influence of exendin-4 intervention on non-obese diabetic (NOD) mouse blood and the pancreatic tissue immune microenvironment. A total of 40 clean NOD mice were used in the study and randomly divided into 4 groups (n=10/group). The first group was blank control group D with normal saline intervention, and with different doses of exendin, i.e.,-4 2, 4 and 8 µg/kg/day. The three remaining groups were: i) Low-dose group A; ii) medium-dose group B; and iii) high-dose group C...
November 2016: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/27880731/smad4-in-t-cells-plays-a-protective-role-in-the-development-of-autoimmune-sj%C3%A3-gren-s-syndrome-in-the-nonobese-diabetic-mouse
#8
Donghee Kim, Jae Young Kim, Hee-Sook Jun
We investigated the role of Smad4, a signaling molecule of the TGF-beta pathway, in T cells on the pathology of Sjögren's syndrome (SS) in nonobese diabetic (NOD) mice, an animal model of SS. T cell-specific Smad4-deleted (Smad4fl/fl,CD4-Cre; Smad4 tKO) NOD mice had accelerated development of SS compared with wild-type (Smad4+/+,CD4-Cre; WT) NOD mice, including increased lymphocyte infiltration into exocrine glands, decreased tear and saliva production, and increased levels of autoantibodies at 12 weeks of age...
November 17, 2016: Oncotarget
https://www.readbyqxmd.com/read/27875342/the-multifaceted-roles-of-inflammasome-proteins-in-cancer
#9
Virginie Petrilli
PURPOSE OF REVIEW: Inflammasomes are major actors of the innate immune system, through their regulation of inflammatory caspases and maturation of IL-1β and IL-18. These multiprotein complexes have been shown to play major roles in inflammatory and metabolic diseases and have more recently been implicated in tumor development and dissemination. In this review, we address these recent findings, focusing particularly on colorectal cancer (CRC) initiation and tumor dissemination. RECENT FINDINGS: Based mostly on loss-of-function experiments in mouse models, paradoxical results were obtained as both protumoral and antitumoral activities were reported...
January 2017: Current Opinion in Oncology
https://www.readbyqxmd.com/read/27872297/singular-role-for-t-bet-cxcr3-regulatory-t-cells-in-protection-from-autoimmune-diabetes
#10
Tze Guan Tan, Diane Mathis, Christophe Benoist
Foxp3(+) regulatory T (Treg) cells are crucial for restraining inflammation in a variety of autoimmune diseases, including type 1 diabetes (T1D). However, the transcriptional and functional phenotypes of Treg cells within the pancreatic lesion remain poorly understood. Here we characterized pancreas-infiltrating Treg cells in the NOD mouse model of T1D and uncovered a substantial enrichment of the Treg subpopulation expressing the chemokine receptor CXCR3. Accumulation of CXCR3(+) Treg cells within pancreatic islets was dependent on the transcription factor T-BET, and genetic ablation of T-BET increased the onset and penetrance of disease, abrogating the sex bias normally seen in the NOD model...
November 21, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27865798/adoptive-transfer-of-ex%C3%A2-vivo-expanded-v%C3%AE-9v%C3%AE-2-t-cells-in-combination-with-zoledronic-acid-inhibits-cancer-growth-and-limits-osteolysis-in-a-murine-model-of-osteolytic-breast-cancer
#11
Aneta Zysk, Mark O DeNichilo, Vasilios Panagopoulos, Irene Zinonos, Vasilios Liapis, Shelley Hay, Wendy Ingman, Vladimir Ponomarev, Gerald Atkins, David Findlay, Andrew Zannettino, Andreas Evdokiou
Bone metastases occur in over 75% of patients with advanced breast cancer and are responsible for high levels of morbidity and mortality. In this study, ex vivo expanded cytotoxic Vγ9Vδ2 T cells isolated from human peripheral blood were tested for their anti-cancer efficacy in combination with zoledronic acid (ZOL), using a mouse model of osteolytic breast cancer. In vitro, expanded Vγ9Vδ2 T cells were cytotoxic against a panel of human breast cancer cell lines, and ZOL pre-treatment further sensitised breast cancer cells to killing by Vγ9Vδ2 T cells...
November 16, 2016: Cancer Letters
https://www.readbyqxmd.com/read/27862942/a-novel-xenogeneic-graft-versus-host-disease-model-for-investigating-the-pathological-role-of-human-cd4-or-cd8-t-cells-using-immunodeficient-nog-mice
#12
Ryoji Ito, Ikumi Katano, Kenji Kawai, Mika Yagoto, Takeshi Takahashi, Yuyo Ka, Tomoyuki Ogura, Riichi Takahashi, Mamoru Ito
Graft-versus-host disease (GVHD) is a major complication of allogenic bone marrow transplantation and involves the infiltration of donor CD4+ and/or CD8+ T cells into various organs of the recipient. The pathological role of human CD4+ and CD8+ T cells in GVHD remains controversial. In this study, we established two novel xenogeneic (xeno)-GVHD models. Human CD4+ or CD8+ T cells were purified from peripheral blood and were transplanted into immunodeficient NOD/Shi-scid IL2rg(null) (NOG) mice. Human CD8+ T cells did not induce major GVHD symptoms in conventional NOG mice...
November 15, 2016: American Journal of Transplantation
https://www.readbyqxmd.com/read/27853735/two-stage-nanoparticle-delivery-of-piperlongumine-and-tumor-necrosis-factor-related-apoptosis-inducing-ligand-trail-anti-cancer-therapy
#13
Charles C Sharkey, Jiahe Li, Sweta Roy, Qianhui Wu, Michael R King
This study outlines a drug delivery mechanism that utilizes two independent vehicles, allowing for delivery of chemically and physically distinct agents. The mechanism was utilized to deliver a new anti-cancer combination therapy consisting of piperlongumine (PL) and TRAIL to treat PC3 prostate cancer and HCT116 colon cancer cells. PL, a small-molecule hydrophobic drug, was encapsulated in poly (lactic-co-glycolic acid) (PLGA) nanoparticles. TRAIL was chemically conjugated to the surface of liposomes. PL was first administered to sensitize cancer cells to the effects of TRAIL...
March 2016: Technology
https://www.readbyqxmd.com/read/27852702/gas6-axl-signaling-regulates-self-renewal-of-chronic-myelogenous-leukemia-stem-cells-by-stabilizing-%C3%AE-catenin
#14
Yanli Jin, Danian Nie, Juan Li, Xin Du, Yuhong Lu, Yangqiu Li, Chang Liu, Jingfeng Zhou, Jingxuan Pan
PURPOSE: Quiescent leukemia stem cells (LSCs) are important resources of resistance and relapse in chronic myelogenous leukemia (CML). Thus, strategies eradicating CML LSCs are required for cure. In this study, we discovered that AXL tyrosine kinase was selectively overexpressed in primary CML CD34+ cells. However, the role of AXL and its ligand Gas6 secreted by stromal cells in the regulation of self-renewal capacity of LSCs has not been well investigated. EXPERIMENTAL DESIGN: The function of CML CD34+ cells was evaluated by flow cytometer, CFC/replating, long-term culture-initiating cells (LTC-IC), CML mouse model driven by human BCR-ABL gene and NOD-scid-IL2Rg-/- (NSI) mice...
November 16, 2016: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/27834793/b-cell-receptor-affinity-for-insulin-dictates-autoantigen-acquisition-and-b-cell-functionality-in-autoimmune-diabetes
#15
Thomas A Packard, Mia J Smith, Francis J Conrad, Sara A Johnson, Andrew Getahun, Robin S Lindsay, Rochelle M Hinman, Rachel S Friedman, James W Thomas, John C Cambier
B cells have been strongly implicated in the development of human type 1 diabetes and are required for disease in the NOD mouse model. These functions are dependent on B cell antigen receptor (BCR) specificity and expression of MHC, implicating linked autoantigen recognition and presentation to effector T cells. BCR-antigen affinity requirements for participation in disease are unclear. We hypothesized that BCR affinity for the autoantigen insulin differentially affects lymphocyte functionality, including tolerance modality and the ability to acquire and become activated in the diabetogenic environment...
November 8, 2016: Journal of Clinical Medicine
https://www.readbyqxmd.com/read/27808091/growth-inhibition-of-cytosolic-salmonella-by-caspase-1-and-caspase-11-precedes-host-cell-death
#16
Teresa L M Thurston, Sophie A Matthews, Elliott Jennings, Eric Alix, Feng Shao, Avinash R Shenoy, Mark A Birrell, David W Holden
Sensing bacterial products in the cytosol of mammalian cells by NOD-like receptors leads to the activation of caspase-1 inflammasomes, and the production of the pro-inflammatory cytokines interleukin (IL)-18 and IL-1β. In addition, mouse caspase-11 (represented in humans by its orthologs, caspase-4 and caspase-5) detects cytosolic bacterial LPS directly. Activation of caspase-1 and caspase-11 initiates pyroptotic host cell death that releases potentially harmful bacteria from the nutrient-rich host cell cytosol into the extracellular environment...
November 3, 2016: Nature Communications
https://www.readbyqxmd.com/read/27802879/an-insulin-iapp-hybrid-peptide-is-an-endogenous-antigen-for-cd4-t-cells-in-the-non-obese-diabetic-mouse
#17
Timothy A Wiles, Thomas Delong, Rocky L Baker, Brenda Bradley, Gene Barbour, Roger L Powell, Nichole Reisdorph, Kathryn Haskins
BDC-6.9, a diabetogenic CD4 T cell clone isolated from a non-obese diabetic (NOD) mouse, responds to pancreatic islet cells from NOD but not BALB/c mice. We recently reported that a hybrid insulin peptide (HIP), 6.9HIP, formed by linkage of an insulin C-peptide fragment and a fragment of islet amyloid polypeptide (IAPP), is the antigen for BDC-6.9. We report here that the core 12-mer peptide from 6.9HIP, centered on the hybrid peptide junction, is also highly antigenic for BDC-6.9. In agreement with the observation that BALB/c islet cells fail to stimulate the T cell clone, a single amino acid difference in the BALB/c IAPP sequence renders the BALB/c version of the HIP only weakly antigenic...
October 29, 2016: Journal of Autoimmunity
https://www.readbyqxmd.com/read/27800616/nlrp12-negatively-regulates-proinflammatory-cytokine-production-and-host-defense-against-brucella-abortus
#18
Tatiana N Silveira, Marco Túlio R Gomes, Luciana S Oliveira, Priscila C Campos, Gabriela G Machado, Sergio C Oliveira
Brucella abortus is the causative agent of brucellosis, which causes abortion in domestic animals and undulant fever in humans. This bacterium infects and proliferates mainly in macrophages and dendritic cells, where it is recognized by pattern recognition receptors (PRRs) including Nod-like receptors (NLRs). Our group recently demonstrated the role of AIM2 and NLRP3 in Brucella recognition. Here, we investigated the participation of NLRP12 in innate immune response to B. abortus. We show that NLRP12 inhibits the early production of IL-12 by bone marrow-derived macrophages upon B...
November 1, 2016: European Journal of Immunology
https://www.readbyqxmd.com/read/27797173/dipeptidyl-vinyl-sulfone-as-a-novel-chemical-tool-to-inhibit-hmgb1-nlrp3-inflammasome-and-inflamma-mirs-in-a%C3%AE-mediated-microglial-inflammation
#19
Ana Sofia Falcão, Luís A R Carvalho, Gonçalo Lidónio, Ana Rita Vaz, Susana Dias Lucas, Rui Moreira, Dora Brites
Rapid microglial activation and associated inflammatory pathways contribute to immune-defense and tissue repair in the central nervous system (CNS). However, persistent activation of these cells will ultimately result in vast production of pro-inflammatory mediators and other neurotoxic factors, which may induce neuronal damage and contribute to chronic neurodegenerative diseases, as Alzheimer's disease (AD). Therefore, small molecules with immunomodulatory effects on microglia may be considered as potential tools to counteract their pro-inflammatory phenotype and neuroimmune dysregulation in such disorders...
October 31, 2016: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/27796442/congenic-mapping-identifies-a-novel-idd9-subregion-regulating-type-1-diabetes-in-nod-mice
#20
Bixuan Lin, Ashley E Ciecko, Erin MacKinney, David V Serreze, Yi-Guang Chen
Type 1 diabetes (T1D) results from complex interactions between genetic and environmental factors. The nonobese diabetic (NOD) mouse develops spontaneous T1D and has been used extensively to study the genetic control of this disease. T1D is suppressed in NOD mice congenic for the C57BL/10 (B10)-derived Idd9 resistance region on chromosome 4. Previous studies conducted by other investigators have identified four subregions (Idd9.1, Idd9.2, Idd9.3, and Idd9.4) where B10-derived genes suppress T1D development in NOD mice...
October 28, 2016: Immunogenetics
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