NDLI: Suppression of the NF-κB pathway by diesel exhaust particles impairs human antimycobacterial immunity.

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: 2012 Volume: 189

Year: 2012 Volume: 188

Year: 2012 Volume: 188 Issue: 12

Year: 2012 Volume: 188 Issue: 11

Year: 2012 Volume: 188 Issue: 10

Year: 2012 Volume: 188 Issue: 9

Year: 2012 Volume: 188 Issue: 8

Year: 2012 Volume: 188 Issue: 7

Year: 2012 Volume: 188 Issue: 6

Factor VII-activating protease is activated in multiple trauma patients and generates anaphylatoxin C5a.

Derivation and maintenance of virtual memory CD8 T cells.

A novel NKR-P1B(bright) NK cell subset expresses an activated CD25(+)CX(3)CR1(+)CD62L(-)CD11b(-)CD27(-) phenotype and is prevalent in blood, liver, and gut-associated lymphoid organs of rats.

Tyrosine phosphorylation-independent regulation of lipopolysaccharide-mediated response by the transmembrane adaptor protein LAB.

Removal of syndecan-1 promotes TRAIL-induced apoptosis in myeloma cells.

Recognition and prevention of tumor metastasis by the NK receptor NKp46/NCR1.

Chronic shift-lag alters the circadian clock of NK cells and promotes lung cancer growth in rats.

TLR4-mediated AKT activation is MyD88/TRIF dependent and critical for induction of oxidative phosphorylation and mitochondrial transcription factor A in murine macrophages.

TREM2 and ß-catenin regulate bone homeostasis by controlling the rate of osteoclastogenesis.

Three novel acetylation sites in the Foxp3 transcription factor regulate the suppressive activity of regulatory T cells.

Cellular and molecular requirements for rejection of B16 melanoma in the setting of regulatory T cell depletion and homeostatic proliferation.

Spatiotemporal inhibition of innate immunity signaling by the Tbc1d23 RAB-GAP.

Selective dependence of H2-M3-restricted CD8 responses on IL-15.

The adaptor protein SLP-76 regulates HIV-1 release and cell-to-cell transmission in T cells.

E3 ubiquitin ligase tripartite motif 38 negatively regulates TLR-mediated immune responses by proteasomal degradation of TNF receptor-associated factor 6 in macrophages.

Cutting edge: the 'death' adaptor CRADD/RAIDD targets BCL10 and suppresses agonist-induced cytokine expression in T lymphocytes.

Analysis of NLRP3 in the development of allergic airway disease in mice.

The impact of a large and frequent deletion in the human TCR ß locus on antiviral immunity.

Midkine inhibits inducible regulatory T cell differentiation by suppressing the development of tolerogenic dendritic cells.

Stromal TIMP3 regulates liver lymphocyte populations and provides protection against Th1 T cell-driven autoimmune hepatitis.

A new hypersensitive site, HS10, and the enhancers E3′ and Ed, differentially regulate Igκ gene expression

Germinal center alloantibody responses are mediated exclusively by indirect-pathway CD4 T follicular helper cells.

Downregulation of the Na/K-ATPase pump by leptospiral glycolipoprotein activates the NLRP3 inflammasome.

A TRIF-independent branch of TLR3 signaling.

Targeting TNF- to neoangiogenic vessels enhances lymphocyte infiltration in tumors and increases the therapeutic potential of immunotherapy.

Alternaria induces STAT6-dependent acute airway eosinophilia and epithelial FIZZ1 expression that promotes airway fibrosis and epithelial thickness.

Cutting edge: the role of IFN- receptor and MyD88 signaling in induction of IL-15 expression in vivo.

Frequency of epitope-specific naive CD4(+) T cells correlates with immunodominance in the human memory repertoire.

JAB1 is essential for B cell development and germinal center formation and inversely regulates Fas ligand and Bcl6 expression.

Innate NK cells and macrophages recognize and reject allogeneic nonself in vivo via different mechanisms.

Cutting edge: paradoxical roles of BST2/tetherin in promoting type I IFN response and viral infection.

Class B scavenger receptor types I and II and CD36 targeting improves sepsis survival and acute outcomes in mice.

The tick salivary protein sialostatin L inhibits the Th9-derived production of the asthma-promoting cytokine IL-9 and is effective in the prevention of experimental asthma.

Impaired NLRP3 inflammasome function in elderly mice during influenza infection is rescued by treatment with nigericin.

Modulation of antigen presentation and B cell receptor signaling in B cells of beige mice.

The development of colitogenic CD4(+) T cells is regulated by IL-7 in collaboration with NK cell function in a murine model of colitis.

Significant role of IL-1 signaling, but limited role of inflammasome activation, in oviduct pathology during Chlamydia muridarum genital infection.

IκB kinase ß is required for activation of NF-κB and AP-1 in CD3/CD28-stimulated primary CD4(+) T cells.

Neonatal rhinovirus infection induces mucous metaplasia and airways hyperresponsiveness.

Adiponectin induces dendritic cell activation via PLCÎ³/JNK/NF-κB pathways, leading to Th1 and Th17 polarization.

Suppression of the NF-κB pathway by diesel exhaust particles impairs human antimycobacterial immunity.

Human cytomegalovirus UL40 signal peptide regulates cell surface expression of the NK cell ligands HLA-E and gpUL18.

Hapivirins and Diprovirins: Novel θ-Defensin Analogs With Potent Activity Against Influenza A $Virus^{}$

Maximal adjuvant activity of nasally delivered IL-1 requires adjuvant-responsive CD11c(+) cells and does not correlate with adjuvant-induced in vivo cytokine production.

Germline deletion of Igh 3' regulatory region elements hs 5, 6, 7 (hs5-7) affects B cell-specific regulation, rearrangement, and insulation of the Igh locus.

Characterization of a PIAS4 homologue from zebrafish: insights into its conserved negative regulatory mechanism in the TRIF, MAVS, and IFN signaling pathways during vertebrate evolution.

MHC class II tetramers.

Year: 2012 Volume: 188 Issue: 5

Year: 2012 Volume: 188 Issue: 4

Year: 2012 Volume: 188 Issue: 3

Year: 2012 Volume: 188 Issue: 2

Year: 2012 Volume: 188 Issue: 1

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

Suppression of the NF-κB pathway by diesel exhaust particles impairs human antimycobacterial immunity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sarkar, Srijata Sarkar, Somak Zhang, Junfeng Song, Youngmia Laumbach, Robert J. Kipen, Howard M. Schwander, Stephan Strickland, Pamela A. Ohman Gardner, Carol R.
Description	Country affiliation: United States Author Affiliation: Sarkar S ( Department of Environmental and Occupational Health, University of Medicine and Dentistry of New Jersey-School of Public Health, Piscataway, NJ 08854, USA.)
Abstract	Epidemiological studies suggest that chronic exposure to air pollution increases susceptibility to respiratory infections, including tuberculosis in humans. A possible link between particulate air pollutant exposure and antimycobacterial immunity has not been explored in human primary immune cells. We hypothesized that exposure to diesel exhaust particles (DEP), a major component of urban fine particulate matter, suppresses antimycobacterial human immune effector cell functions by modulating TLR-signaling pathways and NF-κB activation. We show that DEP and H37Ra, an avirulent laboratory strain of Mycobacterium tuberculosis, were both taken up by the same peripheral human blood monocytes. To examine the effects of DEP on M. tuberculosis-induced production of cytokines, PBMC were stimulated with DEP and M. tuberculosis or purified protein derivative. The production of M. tuberculosis and purified protein derivative-induced IFN-Î³, TNF- , IL-1ß, and IL-6 was reduced in a DEP dose-dependent manner. In contrast, the production of anti-inflammatory IL-10 remained unchanged. Furthermore, DEP stimulation prior to M. tuberculosis infection altered the expression of TLR3, -4, -7, and -10 mRNAs and of a subset of M. tuberculosis-induced host genes including inhibition of expression of many NF-κB (e.g., CSF3, IFNG, IFNA, IFNB, IL1A, IL6, and NFKBIA) and IFN regulatory factor (e.g., IFNG, IFNA1, IFNB1, and CXCL10) pathway target genes. We propose that DEP downregulate M. tuberculosis-induced host gene expression via MyD88-dependent (IL6, IL1A, and PTGS2) as well as MyD88-independent (IFNA, IFNB) pathways. Prestimulation of PBMC with DEP suppressed the expression of proinflammatory mediators upon M. tuberculosis infection, inducing a hyporesponsive cellular state. Therefore, DEP alters crucial components of antimycobacterial host immune responses, providing a possible mechanism by which air pollutants alter antimicrobial immunity.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1101380
Journal	The Journal of Immunology
Issue Number	6
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-03-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Monocytes Immunology Microbiology Nf-kappa B Particulate Matter Adverse Effects Tuberculosis Vehicle Emissions Toxicity Apoptosis Cell Survival Gene Expression Regulation Microscopy, Electron, Transmission Mycobacterium Tuberculosis Metabolism Real-time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Research Support, N.i.h., Extramural 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