NDLI: Airway uric acid is a sensor of inhaled protease allergens and initiates type 2 immune responses in respiratory mucosa.

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: 2014 Volume: 192 Issue: 12

Year: 2014 Volume: 192 Issue: 11

Year: 2014 Volume: 192 Issue: 10

Year: 2014 Volume: 192 Issue: 9

Integrin 4ß1 is necessary for CD4+ T cell-mediated protection against genital Chlamydia trachomatis infection.

TLR4 ligands lipopolysaccharide and monophosphoryl lipid a differentially regulate effector and memory CD8+ T Cell differentiation.

Mycobacterium tuberculosis impairs dendritic cell functions through the serine hydrolase Hip1.

Multiple CD11c+ cells collaboratively express IL-1ß to modulate stromal vascular endothelial growth factor and lymph node vascular-stromal growth.

Reduced regulatory T cell diversity in NOD mice is linked to early events in the thymus.

A novel mechanism underlying the basic defensive response of macrophages against Mycobacterium infection.

Airway uric acid is a sensor of inhaled protease allergens and initiates type 2 immune responses in respiratory mucosa.

Interplay between CXCR2 and BLT1 facilitates neutrophil infiltration and resultant keratinocyte activation in a murine model of imiquimod-induced psoriasis.

1,25-Dihydroxyvitamin D3 promotes tolerogenic dendritic cells with functional migratory properties in NOD mice.

A critical role for thymic stromal lymphopoietin in nickel-induced allergy in mice.

Congenital heart disease linked to maternal autoimmunity against cardiac myosin.

Synergistic therapeutic vascular cytoprotection against complement-mediated injury induced via a PKC -, AMPK-, and CREB-dependent pathway.

Conservation of pathogenic TCR homology across class II restrictions in anti-ribonucleoprotein autoimmunity: extended efficacy of T cell vaccine therapy.

Regulatory CD4+ T cells promote B cell anergy in murine lupus.

BAFF suppresses IL-15 expression in B cells.

Engineering of a novel anti-CD40L domain antibody for treatment of autoimmune diseases.

ß7 Integrin controls mast cell recruitment, whereas E integrin modulates the number and function of CD8+ T cells in immune complex-mediated tissue injury.

Inhibition of GTPase Rac1 in endothelium by 6-mercaptopurine results in immunosuppression in nonimmune cells: new target for an old drug.

Engagement of SLAMF2/CD48 prolongs the time frame of effective T cell activation by supporting mature dendritic cell survival.

Age-enhanced endoplasmic reticulum stress contributes to increased Atg9A inhibition of STING-mediated IFN-ß production during Streptococcus pneumoniae infection.

HLA-DR 1 constructs block CD74 expression and MIF effects in experimental autoimmune encephalomyelitis.

Cell depletion in mice that express diphtheria toxin receptor under the control of SiglecH encompasses more than plasmacytoid dendritic cells.

Contrasted innate responses to two viruses in zebrafish: insights into the ancestral repertoire of vertebrate IFN-stimulated genes.

Molecular mechanisms of TLR2-mediated antigen cross-presentation in dendritic cells.

Altered expression of oligodendrocyte and neuronal marker genes predicts the clinical onset of autoimmune encephalomyelitis and indicates the effectiveness of multiple sclerosis-directed therapeutics.

Periodontal pathogens directly promote autoimmune experimental arthritis by inducing a TLR2- and IL-1-driven Th17 response.

Mechanistic target of rapamycin complex 1 expands Th17 and IL-4+ CD4-CD8- double-negative T cells and contracts regulatory T cells in systemic lupus erythematosus.

NKT cells determine titer and subtype profile of virus-specific IgG antibodies during herpes simplex virus Infection.

Heterocomplex formation between MBL/ficolin/CL-11-associated serine protease-1 and -3 and MBL/ficolin/CL-11-associated protein-1.

TCR bias and affinity define two compartments of the CD1b-glycolipid-specific T Cell repertoire.

Differential ability of surface and endosomal TLRs to induce CD8 T cell responses in vivo.

CTLA-4 is expressed by activated mouse NK cells and inhibits NK Cell IFN-Î³ production in response to mature dendritic cells.

Immunological priming requires regulatory T cells and IL-10-producing macrophages to accelerate resolution from severe lung inflammation.

TLR-mediated secretion of endoplasmic reticulum aminopeptidase 1 from macrophages.

JAK2-STAT3 blockade by AG490 suppresses autoimmune arthritis in mice via reciprocal regulation of regulatory T Cells and Th17 cells.

High molecular weight kininogen binds phosphatidylserine and opsonizes urokinase plasminogen activator receptor-mediated efferocytosis.

SAP facilitates recruitment and activation of LCK at NTB-A receptors during restimulation-induced cell death.

The influenza virus-specific CTL immunodominance hierarchy in mice is determined by the relative frequency of high-avidity T cells.

CD20+ B cell depletion alters T cell homing.

Rab5 is a novel regulator of mast cell secretory granules: impact on size, cargo, and exocytosis.

Soluble IFN receptor potentiates in vivo type I IFN signaling and exacerbates TLR4-mediated septic shock.

NLRP3 regulates neutrophil functions and contributes to hepatic ischemia-reperfusion injury independently of inflammasomes.

Naive idiotope-specific B and T cells collaborate efficiently in the absence of dendritic cells.

Wnt5a-Rac1-NF-κB homeostatic circuitry sustains innate immune functions in macrophages.

Human procaspase-1 variants with decreased enzymatic activity are associated with febrile episodes and may contribute to inflammation via RIP2 and NF-κB signaling.

Response to comment on 'killer Ig-like receptor 2DL4 does not mediate NK cell IFN-Î³ responses to soluble HLA-G preparations'.

Development and implementation of papillomavirus prophylactic vaccines.

A clue to antigen receptor tails.

An overview of the intrathymic intricacies of T cell development.

Year: 2014 Volume: 192 Issue: 8

Year: 2014 Volume: 192 Issue: 7

Year: 2014 Volume: 192 Issue: 6

Year: 2014 Volume: 192 Issue: 5

Year: 2014 Volume: 192 Issue: 4

Year: 2014 Volume: 192 Issue: 3

Year: 2014 Volume: 192 Issue: 2

Year: 2014 Volume: 192 Issue: 1

Year: 2013 Volume: 191

Year: 2013 Volume: 190

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

Airway uric acid is a sensor of inhaled protease allergens and initiates type 2 immune responses in respiratory mucosa.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Iijima, Koji Elias, Martha K. Kobayashi, Takao Hara, Kenichiro Kurabayashi, Masahiko Seno, Satoshi Kita, Hirohito Tojima, Ichiro Kephart, Gail M.
Description	Author Affiliation: Hara K ( Division of Allergic Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, MN 55905)
Abstract	Although type 2 immune responses to environmental Ags are thought to play pivotal roles in asthma and allergic airway diseases, the immunological mechanisms that initiate the responses are largely unknown. Many allergens have biologic activities, including enzymatic activities and abilities to engage innate pattern-recognition receptors such as TLR4. In this article, we report that IL-33 and thymic stromal lymphopoietin were produced quickly in the lungs of naive mice exposed to cysteine proteases, such as bromelain and papain, as a model for allergens. IL-33 and thymic stromal lymphopoietin sensitized naive animals to an innocuous airway Ag OVA, which resulted in production of type 2 cytokines and IgE Ab, and eosinophilic airway inflammation when mice were challenged with the same Ag. Importantly, upon exposure to proteases, uric acid (UA) was rapidly released into the airway lumen, and removal of this endogenous UA by uricase prevented type 2 immune responses. UA promoted secretion of IL-33 by airway epithelial cells in vitro, and administration of UA into the airways of naive animals induced extracellular release of IL-33, followed by both innate and adaptive type 2 immune responses in vivo. Finally, a potent UA synthesis inhibitor, febuxostat, mitigated asthma phenotypes that were caused by repeated exposure to natural airborne allergens. These findings provide mechanistic insights into the development of type 2 immunity to airborne allergens and recognize airway UA as a key player that regulates the process in respiratory mucosa.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400110
Journal	The Journal of Immunology
Issue Number	9
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adaptive Immunity Immunology Allergens Peptide Hydrolases Respiratory Mucosa Uric Acid Animals Bromelains Pharmacology Cytokines Biosynthesis Disease Models, Animal Enzyme-linked Immunosorbent Assay Flow Cytometry Interleukin-33 Interleukins Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Microscopy, Confocal Papain Pneumonia Metabolism Th2 Cells 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