NDLI: AMP-activated protein kinase restricts IFN-Î³ signaling.

Please wait, while we are loading the content...

Year: 2017 Volume: 198

Year: 2016 Volume: 197

Year: 2016 Volume: 196

Year: 2015 Volume: 195

Year: 2015 Volume: 194

Year: 2014 Volume: 193

Year: 2014 Volume: 192

Year: 2013 Volume: 191

Year: 2013 Volume: 190

Year: 2013 Volume: 190 Issue: 12

Year: 2013 Volume: 190 Issue: 11

Year: 2013 Volume: 190 Issue: 10

Year: 2013 Volume: 190 Issue: 9

Year: 2013 Volume: 190 Issue: 8

Year: 2013 Volume: 190 Issue: 7

Year: 2013 Volume: 190 Issue: 6

Year: 2013 Volume: 190 Issue: 5

Year: 2013 Volume: 190 Issue: 4

Year: 2013 Volume: 190 Issue: 3

Year: 2013 Volume: 190 Issue: 2

Year: 2013 Volume: 190 Issue: 1

An HLA-DRB1-coded signal transduction ligand facilitates inflammatory arthritis: a new mechanism of autoimmunity.

Phosphatidylinositol 3-kinase-Î³ signaling promotes Campylobacter jejuni-induced colitis through neutrophil recruitment in mice.

Phosphoinositide 3-OH kinase regulates integrin-dependent processes in neutrophils by signaling through its effector ARAP3.

TLR9-dependent IL-23/IL-17 is required for the generation of Stachybotrys chartarum-induced hypersensitivity pneumonitis.

TIM-3 regulates innate immune cells to induce fetomaternal tolerance.

AMP-activated protein kinase restricts IFN-Î³ signaling.

Enzymatic discovery of a HER-2/neu epitope that generates cross-reactive T cells.

Impact of IgA constant domain on HIV-1 neutralizing function of monoclonal antibody F425A1g8.

Identification of lineage relationships and novel markers of blood and skin human dendritic cells.

SLAT regulates CD8+ T cell clonal expansion in a Cdc42- and NFAT1-dependent manner.

YKL-40 induces IL-8 expression from bronchial epithelium via MAPK (JNK and ERK) and NF-κB pathways, causing bronchial smooth muscle proliferation and migration.

Lipoproteins are major targets of the polyclonal human T cell response to Mycobacterium tuberculosis.

MARCO is required for TLR2- and Nod2-mediated responses to Streptococcus pneumoniae and clearance of pneumococcal colonization in the murine nasopharynx.

Multiple redundant effector mechanisms of CD8+ T cells protect against influenza infection.

CD47 deficiency does not impede polymorphonuclear neutrophil transmigration but attenuates granulopoiesis at the postacute stage of colitis.

Cleavage of anti-apoptotic Bcl-2 family members after TCR stimulation contributes to the decision between T cell activation and apoptosis.

Early growth response gene-2 controls IL-17 expression and Th17 differentiation by negatively regulating Batf.

FcÎ³RIIb on myeloid cells and intrinsic renal cells rather than B cells protects from nephrotoxic nephritis.

Memory CD4+ T cells are required for optimal NK cell effector functions against the opportunistic fungal pathogen Pneumocystis murina.

Dermatophagoides pteronyssinus major allergen 1 activates the innate immune response of the fruit fly Drosophila melanogaster.

Reduced surface expression of TLR4 by a V254I point mutation accounts for the low lipopolysaccharide responder phenotype of BALB/c B cells.

Association between magnitude of the virus-specific plasmablast response and disease severity in dengue patients.

Effective cooperation of monoclonal antibody and peptide vaccine for the treatment of mouse melanoma.

Unraveling graft-versus-host disease and graft-versus-leukemia responses using TCR Vß spectratype analysis in a murine bone marrow transplantation model.

A phospholipase C-Î³1-independent, RasGRP1-ERK-dependent pathway drives lymphoproliferative disease in linker for activation of T cells-Y136F mutant mice.

CD11b/CD18 (Mac-1) is a novel surface receptor for extracellular double-stranded RNA to mediate cellular inflammatory responses.

Central role for endothelial human deneddylase-1/SENP8 in fine-tuning the vascular inflammatory response.

Complete dependence on IRAK4 kinase activity in TLR2, but not TLR4, signaling pathways underlies decreased cytokine production and increased susceptibility to Streptococcus pneumoniae infection in IRAK4 kinase-inactive mice.

Quorum sensing contributes to activated IgM-secreting B cell homeostasis.

Immunodeficiency and autoimmunity in H2-O-deficient mice.

TLR3, TRIF, and caspase 8 determine double-stranded RNA-induced epithelial cell death and survival in vivo.

Rho-family GTPase Cdc42 controls migration of Langerhans cells in vivo.

In vivo blockade of the PD-1 receptor suppresses HIV-1 viral loads and improves CD4+ T cell levels in humanized mice.

A novel domain cassette identifies Plasmodium falciparum PfEMP1 proteins binding ICAM-1 and is a target of cross-reactive, adhesion-inhibitory antibodies.

A pathogenic role for CD4+ T cells during Chikungunya virus infection in mice.

Ofatumumab is more efficient than rituximab in lysing B chronic lymphocytic leukemia cells in whole blood and in combination with chemotherapy.

Toward animal cell culture-based influenza vaccine design: viral hemagglutinin N-glycosylation markedly impacts immunogenicity.

G i2 is the essential G i protein in immune complex-induced lung disease.

GATA-3 regulates the homeostasis and activation of CD8+ T cells.

Nuclear translocation of MEK1 triggers a complex T cell response through the corepressor silencing mediator of retinoid and thyroid hormone receptor.

Blocking A2B adenosine receptor alleviates pathogenesis of experimental autoimmune encephalomyelitis via inhibition of IL-6 production and Th17 differentiation.

Apoptotic programs are determined during lineage commitment of CD4+ T effectors: selective regulation of T effector-memory apoptosis by inducible nitric oxide synthase.

TLR agonists stimulate Nlrp3-dependent IL-1ß production independently of the purinergic P2X7 receptor in dendritic cells and in vivo.

Cutting edge: Ly9 (CD229), a SLAM family receptor, negatively regulates the development of thymic innate memory-like CD8+ T and invariant NKT cells.

Isolation of human CD4/CD8 double-positive, graft-versus-host disease-protective, minor histocompatibility antigen-specific regulatory T cells and of a novel HLA-DR7-restricted HY-specific CD4 clone.

In vivo processing of CXCL5 (LIX) by matrix metalloproteinase (MMP)-2 and MMP-9 promotes early neutrophil recruitment in IL-1ß-induced peritonitis.

Immune-mediated regression of established B16F10 melanoma by intratumoral injection of attenuated Toxoplasma gondii protects against rechallenge

Adenosine A2A receptor agonist-mediated increase in donor-derived regulatory T cells suppresses development of graft-versus-host disease.

IFN-Î³ from CD4 T cells is essential for host survival and enhances CD8 T cell function during Mycobacterium tuberculosis infection.

Antibody binding to Cryptococcus neoformans impairs budding by altering capsular mechanical properties.

Increasing viral dose causes a reversal in CD8+ T cell immunodominance during primary influenza infection due to differences in antigen presentation, T cell avidity, and precursor numbers.

MyD88: a critical adaptor protein in innate immunity signal transduction.

Year: 2012 Volume: 189

Year: 2012 Volume: 188

Year: 2011 Volume: 187

Year: 2011 Volume: 186

Year: 2010 Volume: 185

Year: 2010 Volume: 184

Year: 2009 Volume: 183

Year: 2009 Volume: 182

Year: 2008 Volume: 181

AMP-activated protein kinase restricts IFN-Î³ signaling.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Liu, Yudong Qin, Hongwei Benveniste, Etty N. Meares, Gordon P. Holdbrooks, Andrew T.
Description	Country affiliation: United States Author Affiliation: Meares GP ( Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.)
Abstract	Inflammation in the CNS contributes to neurologic disorders. Neuroinflammation involves the release of inflammatory molecules from glial cells, such as astrocytes and microglia, and can lead to neuronal damage if unabated. In multiple sclerosis, peripheral immune cells, including IFN-Î³-producing Th1 cells, infiltrate the CNS and are important in shaping the inflammatory microenvironment, in part through cytokine-mediated interactions with glial cells. Recent evidence suggests that AMP-activated protein kinase (AMPK), a central regulator of energetic metabolism, can regulate inflammatory gene expression. In this study, we identified that IFN-Î³ induces biphasic AMPK signaling, suggestive of negative-feedback mechanisms. Activation of AMPK suppresses several IFN-Î³-induced cytokines and chemokines in primary astrocytes and microglia. IFN-Î³ regulates gene expression through activation of STAT1, and deletion of AMPK results in a marked increase in basal expression of STAT1. Conversely, activation of AMPK blocks IFN-Î³-induced STAT1 expression. Deletion of AMPK leads to increased basal and IFN-Î³-induced expression of inflammatory molecules, including TNF- , CXCL10, and CCL2. AMPK does not affect the phosphorylation of STAT1, but instead attenuates nuclear translocation of STAT1, DNA binding, and subsequent gene expression. In vivo, AMPK signaling during experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis, is downregulated in the brain at onset and peak of disease. Diminution of AMPK signaling in vivo correlates with increased expression of IFN-Î³ and CCL2 in the CNS. Overall, these findings provide the first link between AMPK and STAT1 and may provide important clues about how bioenergetics and inflammation are linked.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202390
Journal	The Journal of Immunology
Issue Number	1
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Amp-activated Protein Kinases Physiology Down-regulation Immunology Interferon-gamma Antagonists & Inhibitors Deficiency Animals Astrocytes Enzymology Metabolism Cells, Cultured Genetics Energy Metabolism Mice Mice, Inbred C57bl Mice, Knockout Microglia Recombinant Proteins Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Central Library (ISO-9001:2015 Certified)
Indian Institute of Technology Kharagpur
Kharagpur, West Bengal, India | PIN - 721302

See location in the Map
03222 282435
Mail: support@ndl.gov.in

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in