NDLI: Reduced caveolin-1 promotes hyperinflammation due to abnormal heme oxygenase-1 localization in lipopolysaccharide-challenged macrophages with dysfunctional cystic fibrosis transmembrane conductance regulator.

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

The influence of T cell Ig mucin-3 signaling on central nervous system autoimmune disease is determined by the effector function of the pathogenic T cells.

Lipopolysaccharide clearance, bacterial clearance, and systemic inflammatory responses are regulated by cell type-specific functions of TLR4 during sepsis.

A phosphatidylinositol species acutely generated by activated macrophages regulates innate immune responses.

Cutting edge: Macrophages are required for localization of antigen-activated B cells to the follicular perimeter and the subsequent germinal center response.

Modulation of mycobacterial-specific Th1 and Th17 cells in latent tuberculosis by coincident hookworm infection.

Neutrophils confer T cell resistance to myeloid-derived suppressor cell-mediated suppression to promote chronic inflammation.

Fine-tuning of regulatory T cell function: the role of calcium signals and naive regulatory T cells for regulatory T cell deficiency in multiple sclerosis.

GARP-TGF-ß complexes negatively regulate regulatory T cell development and maintenance of peripheral CD4+ T cells in vivo.

Neuroblastoma-derived TGF-ß1 modulates the chemokine receptor repertoire of human resting NK cells.

Lymphotoxin ß receptor regulates the development of CCL21-expressing subset of postnatal medullary thymic epithelial cells.

CD43-mediated IFN-Î³ production by CD8+ T cells promotes abdominal aortic aneurysm in mice.

Cannabinoid 1 receptors in keratinocytes modulate proinflammatory chemokine secretion and attenuate contact allergic inflammation.

Acidic amino acid residues in the juxtamembrane region of the nucleotide-sensing TLRs are important for UNC93B1 binding and signaling.

Hepatitis B virus surface antigen selectively inhibits TLR2 ligand-induced IL-12 production in monocytes/macrophages by interfering with JNK activation.

IFNAR1 controls progression to cerebral malaria in children and CD8+ T cell brain pathology in Plasmodium berghei-infected mice.

Mouse, but not human STING, binds and signals in response to the vascular disrupting agent 5,6-dimethylxanthenone-4-acetic acid.

Local 'on-demand' generation and function of antigen-specific Foxp3+ regulatory T cells.

IL-22 deficiency alters colonic microbiota to be transmissible and colitogenic.

Hemorrhagic shock augments Nlrp3 inflammasome activation in the lung through impaired pyrin induction.

Identification of B cell defects using age-defined reference ranges for in vivo and in vitro B cell differentiation.

Regulator of calcineurin 1 suppresses inflammation during respiratory tract infections.

Mesenchymal stem cells tune the development of monocyte-derived dendritic cells toward a myeloid-derived suppressive phenotype through growth-regulated oncogene chemokines.

The survival of memory CD8 T cells that is mediated by IL-15 correlates with sustained protection against malaria.

Control of the STAT6-BCL6 antagonism by SWAP-70 determines IgE production.

Phosphatidylinositol 4-phosphate 5-kinase activation critically contributes to CD28-dependent signaling responses.

Intestinal Lin- c-Kit+ NKp46- CD4- population strongly produces IL-22 upon IL-1ß stimulation.

The NADPH oxidase pathway is dysregulated by the P2X7 receptor in the SOD1-G93A microglia model of amyotrophic lateral sclerosis.

MicroRNA-146a negatively regulates the immunoregulatory activity of bone marrow stem cells by targeting prostaglandin E2 synthase-2.

Role of nucleic acid-sensing TLRs in diverse autoantibody specificities and anti-nuclear antibody-producing B cells.

Butyrophilin Btn2a2 inhibits TCR activation and phosphatidylinositol 3-kinase/Akt pathway signaling and induces Foxp3 expression in T lymphocytes.

CD163 and IgG codefend against cytotoxic hemoglobin via autocrine and paracrine mechanisms.

High viral burden restricts short-lived effector cell number at late times postinfection through increased natural regulatory T cell expansion.

Dopamine receptor D3 expressed on CD4+ T cells favors neurodegeneration of dopaminergic neurons during Parkinson's disease.

TLR activation excludes circulating naive CD8+ T cells from gut-associated lymphoid organs in mice.

G protein-coupled receptor kinase 6 deficiency promotes angiogenesis, tumor progression, and metastasis.

Impaired autophagy, defective T cell homeostasis, and a wasting syndrome in mice with a T cell-specific deletion of Vps34.

IL-17 stimulates differentiation of human anti-inflammatory macrophages and phagocytosis of apoptotic neutrophils in response to IL-10 and glucocorticoids.

HLA haplotype determines hapten or p-i T cell reactivity to flucloxacillin.

Bruton's tyrosine kinase is required for apoptotic cell uptake via regulating the phosphorylation and localization of calreticulin.

Chemokine receptor CXCR6-dependent hepatic NK T Cell accumulation promotes inflammation and liver fibrosis.

Reduced caveolin-1 promotes hyperinflammation due to abnormal heme oxygenase-1 localization in lipopolysaccharide-challenged macrophages with dysfunctional cystic fibrosis transmembrane conductance regulator.

Pin1-FADD interactions regulate Fas-mediated apoptosis in activated eosinophils.

The novel role of IL-7 ligation to IL-7 receptor in myeloid cells of rheumatoid arthritis and collagen-induced arthritis.

Regulation of Th1 cells and experimental autoimmune encephalomyelitis by glycogen synthase kinase-3.

Chromatin architecture, CCCTC-binding factor, and V(D)J recombination: managing long-distance relationships at antigen receptor loci.

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

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

Reduced caveolin-1 promotes hyperinflammation due to abnormal heme oxygenase-1 localization in lipopolysaccharide-challenged macrophages with dysfunctional cystic fibrosis transmembrane conductance regulator.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Murray, Thomas S. Ferrari, Eleonora Esposito, Speranza D'Souza, Anthony Egan, Marie E. Maiuri, Luigi Raia, Valeria Villella, Valeria R. Krause, Diane S. Zhang, Ping-Xia Bruscia, Emanuela M.
Description	Country affiliation: United States Author Affiliation: Zhang PX ( Department of Pediatrics, Yale University School of Medicine, New Haven, CT 06509, USA.)
Abstract	We have previously reported that TLR4 signaling is increased in LPS-stimulated cystic fibrosis (CF) macrophages (MΦs), contributing to the robust production of proinflammatory cytokines. The heme oxygenase-1 (HO-1)/CO pathway modulates cellular redox status, inflammatory responses, and cell survival. The HO-1 enzyme, together with the scaffold protein caveolin 1 (CAV-1), also acts as a negative regulator of TLR4 signaling in MΦs. In this study, we demonstrate that in LPS-challenged CF MΦs, HO-1 does not compartmentalize normally to the cell surface and instead accumulates intracellularly. The abnormal HO-1 localization in CF MΦs in response to LPS is due to decreased CAV-1 expression, which is controlled by the cellular oxidative state, and is required for HO-1 delivery to the cell surface. Overexpression of HO-1 or stimulating the pathway with CO-releasing molecules enhances CAV-1 expression in CF MΦs, suggesting a positive-feed forward loop between HO-1/CO induction and CAV-1 expression. These manipulations re-established HO-1 and CAV-1 cell surface localization in CF MΦs. Consistent with restoration of HO-1/CAV-1-negative regulation of TLR4 signaling, genetic or pharmacological (CO-releasing molecule 2) induced enhancement of this pathway decreased the inflammatory response of CF MΦs and CF mice treated with LPS. In conclusion, our results demonstrate that the counterregulatory HO-1/CO pathway, which is critical in balancing and limiting the inflammatory response, is defective in CF MΦs through a CAV-1-dependent mechanism, exacerbating the CF MΦ response to LPS. This pathway could be a potential target for therapeutic intervention for CF lung disease.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201607
Journal	The Journal of Immunology
Issue Number	10
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-05-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Caveolin 1 Metabolism Cystic Fibrosis Transmembrane Conductance Regulator Heme Oxygenase-1 Macrophages Immunology Adolescent Animals Biosynthesis Cells, Cultured Child, Preschool Cystic Fibrosis Genetics Inflammation Lipopolysaccharides Lung Diseases Membrane Proteins Mice Mice, Knockout Nasal Polyps Reactive Oxygen Species Signal Transduction Toll-like Receptor 4 Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't 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