73 research outputs found
IL-33 Is Produced by Mast Cells and Regulates IgE-Dependent Inflammation
- Author
- A Lorentz
- A Lorentz
- A Matsuda
- A Mazzoni
- A Oshiba
- A Werman
- AA Chackerian
- AL Rankin
- AM Gilfillan
- AM Gilfillan
- AM Kuchler
- AM Miller
- AU Luthi
- BK Wershil
- C Cayrol
- C Hogaboam
- C Moussion
- Chia-Lin Hsu
- CJ Beltran
- Colleen V. Neilsen
- D Moulin
- D Prefontaine
- D Talabot-Ayer
- Derya Unutmaz
- DS Robinson
- G Haraldsen
- H Matsushima
- H Ochi
- IS Wood
- J Rivera
- J Schmitz
- JD McCurdy
- K Obata
- K Suzuki
- LH Ho
- M Iikura
- M Kaneko
- M Komai-Koma
- M Suzukawa
- MA Rank
- MD Smithgall
- MJ Townsend
- MW Pfaffl
- NE Humphreys
- NI Kang
- Paul J. Bryce
- PJ Bryce
- PN Pushparaj
- SJ Galli
- SJ Galli
- SJ Kim
- T Ohno
- T Pecaric-Petkovic
- V Carriere
- WA Verri Jr
- WB Cherry
- Y Nakamura
- Y Okayama
- Z Allakhverdi
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2010
- Field of study
Background: IL-33 is a recently characterized IL-1 family cytokine and found to be expressed in inflammatory diseases, including severe asthma and inflammatory bowl disease. Recombinant IL-33 has been shown to enhance Th2-associated immune responses and potently increase mast cell proliferation and cytokine production. While IL-33 is constitutively expressed in endothelial and epithelial cells, where it may function as a transcriptional regulator, cellular sources of IL-33 and its role in inflammation remain unclear. Methodology/Principal Findings: Here, we identify mast cells as IL-33 producing cells. IgE/antigen activation of bone marrow-derived mast cells or a murine mast cell line (MC/9) significantly enhanced IL-33. Conversely, recombinant IL-33 directly activated mast cells to produce several cytokines including IL-4, IL-5 and IL-6 but not IL-33. We show that expression of IL-33 in response to IgE-activation required calcium and that ionomycin was sufficient to induce IL-33. In vivo, peritoneal mast cells expressed IL-33 and IL-33 levels were significantly lower within the skin of mast cell deficient mice, compared to littermate controls. Local activation of mast cells promotes edema, followed by the recruitment of inflammatory cells. We demonstrate using passive cutaneous anaphylaxis, a mast cell-dependent model, that deficiency in ST2 or antibody blockage of ST2 or IL-33 ablated the late phase inflammatory response but that the immediate phase response was unaffected. IL-33 levels in the skin were significantly elevated only during the late phase
A rare IL33 loss-of-function mutation reduces blood eosinophil counts and protects from asthma.
- Author
- A Heinzmann
- A Kong
- A Lingel
- A McKenna
- Adalbjorg Jonasdottir
- Ai Ching Lim
- AM Zoltowska
- Andrea Heinzmann
- Asgeir Sigurdsson
- Aslaug Jonasdottir
- B Johnsson
- B Stolarski
- Bjorn Runar Ludviksson
- BK Bulik-Sullivan
- C Trapnell
- C Trapnell
- CC van Diemen
- Celeste Porsbjerg
- DA Loisel
- Daniel F. Gudbjartsson
- David Gislason
- DF Gudbjartsson
- DF Gudbjartsson
- DG Torgerson
- DG Torgerson
- Dirk Smith
- Dora Ludviksdottir
- DS Postma
- E Halapi
- E Lefrancais
- E Lynge
- G Palmer
- G Sveinbjornsson
- Gardar Sveinbjornsson
- Gerard H. Koppelman
- GG Brusselle
- GH Koppelman
- Gisli Masson
- Gudmundur I. Eyjolfsson
- H Jongepier
- H Luo
- H Makrinioti
- H Morita
- H. Marike Boezen
- Hannes Helgason
- Hans Bisgaard
- Haruki Hasegawa
- HY Lee
- Ingileif Jonsdottir
- IS Wood
- Isleifur Olafsson
- IV Kutyavin
- J Schmitz
- J Stoops
- J Wu
- James A. Johnston
- JE Ho
- JN Miller
- Johannes Waage
- JW Hansen
- JW Hansen
- K Bonnelykke
- K Eilbeck
- Kari Stefansson
- Klaus A. Deichmann
- Klaus BĂžnnelykke
- L Akhabir
- Logan Garrett
- Marcus Krueger
- MF Moffatt
- Michael Brown
- Monica Gavala
- NS Grotenboer
- OE Savenije
- Olafur T. Magnusson
- Olof Sigurdardottir
- P Sulem
- Pall Torfi Onundarson
- Patrick Sulem
- Randal R. Ketchem
- S Gretarsdottir
- Tarunveer S. Ahluwalia
- Thorarinn Gislason
- Tuuli Lappalainen
- U Styrkarsdottir
- Unnur Steina Bjornsdottir
- Unnur Thorsteinsdottir
- V Carriere
- V Emilsson
- Vibeke Backer
- W McLaren
- WB Cherry
- Publication venue
- 'Public Library of Science (PLoS)'
- Publication date
- 01/01/2017
- Field of study
Efst ĂĄ sĂĂ°unni er hĂŠgt aĂ° nĂĄlgast greinina Ă heild sinni meĂ° ĂŸvĂ aĂ° smella ĂĄ hlekkinnIL-33 is a tissue-derived cytokine that induces and amplifies eosinophilic inflammation and has emerged as a promising new drug target for asthma and allergic disease. Common variants at IL33 and IL1RL1, encoding the IL-33 receptor ST2, associate with eosinophil counts and asthma. Through whole-genome sequencing and imputation into the Icelandic population, we found a rare variant in IL33 (NM_001199640:exon7:c.487-1G>C (rs146597587-C), allele frequency = 0.65%) that disrupts a canonical splice acceptor site before the last coding exon. It is also found at low frequency in European populations. rs146597587-C associates with lower eosinophil counts (ÎČ = -0.21 SD, P = 2.5Ă10-16, N = 103,104), and reduced risk of asthma in Europeans (OR = 0.47; 95%CI: 0.32, 0.70, P = 1.8Ă10-4, N cases = 6,465, N controls = 302,977). Heterozygotes have about 40% lower total IL33 mRNA expression than non-carriers and allele-specific analysis based on RNA sequencing and phased genotypes shows that only 20% of the total expression is from the mutated chromosome. In half of those transcripts the mutation causes retention of the last intron, predicted to result in a premature stop codon that leads to truncation of 66 amino acids. The truncated IL-33 has normal intracellular localization but neither binds IL-33R/ST2 nor activates ST2-expressing cells. Together these data demonstrate that rs146597587-C is a loss of function mutation and support the hypothesis that IL-33 haploinsufficiency protects against asthma.Netherlands Asthma Foundation University Medical Center Groningen
Ministry of Health and Environmental Hygiene of Netherlands
Netherlands Asthma
Stichting Astma Bestrijding
BBMRI
European Respiratory Society
private and public research funds
AstraZeneca
ALK-Abello, Denmar
Multi-messenger observations of a binary neutron star merger
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- Aab A
- Aartsen MG
- Abbott BP
- Abbott R
- Abbott TD
- Abbott TMC
- Abdalla H
- Abe F
- Abeysekara AU
- Abramo LR
- Abramowski A
- Abreu P
- Acernese F
- Acero F
- Ackermann M
- Ackley K
- Ackley K
- Adams C
- Adams J
- Adams SM
- Adams T
- Addesso P
- Adhikari RX
- Adya VB
- Affeldt C
- Afrough M
- Agarwal B
- Agathos M
- Agatsuma K
- Aggarwal N
- Aglietta M
- Agliozzo C
- Agudo I
- Aguiar OD
- Aguilar JA
- Aharonian F
- Ahlers M
- Ahrens M
- Aiello L
- Ain A
- Ajith P
- Akras S
- Al Samarai I
- Albert A
- Albert A
- Albuquerque IFM
- Albury JM
- Alcaniz JS
- Alexander KD
- Alfaro R
- Alighieri S Di Serego
- Allam S
- Allekotte I
- Allen B
- Allen G
- Allison J
- Allison JR
- Allocca A
- Almela A
- Altin PA
- Altmann D
- Alvarez C
- Alvarez JD
- Alvarez M Dovale
- Alvarez-Muiz J
- Amati L
- Amato A
- An T
- Ananyeva A
- Anastasi GA
- Anchordoqui L
- Andeen K
- Anderson JP
- Anderson SB
- Anderson T
- Anderson WG
- Andrada B
- Andre M
- Andreoni I
- Andreoni I
- Andringa S
- Angelova SV
- Anghinolfi M
- Angner EO
- Angus CR
- Annis J
- Ansseau I
- Antier S
- Anton G
- Antonelli LA
- Antonelli LA
- Anupama GC
- Aoki K
- Aoki W
- Appert S
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- Arai K
- Arakawa M
- Aramo C
- Araya MC
- Arcavi I
- Arceo R
- Ardid M
- Areeda JS
- Aresu G
- Argan A
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- Arnaud N
- Array LWA Long Wavelength
- Array MWA Murchison Widefield
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- Artola R
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- Aulbert C
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- Publication date
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- Field of study
On 2017 August 17 a binary neutron star coalescence candidate (later designated GW170817) with merger time 12:41:04 UTC was observed through gravitational waves by the Advanced LIGO and Advanced Virgo detectors. The Fermi Gamma-ray Burst Monitor independently detected a gamma-ray burst (GRB 170817A) with a time delay of ~1.7 s with respect to the merger time. From the gravitational-wave signal, the source was initially localized to a sky region of 31 deg2 at a luminosity distance of 40+8-8 Mpc and with component masses consistent with neutron stars. The component masses were later measured to be in the range 0.86 to 2.26 Mo. An extensive observing campaign was launched across the electromagnetic spectrum leading to the discovery of a bright optical transient (SSS17a, now with the IAU identification of AT 2017gfo) in NGC 4993 (at ~40 Mpc) less than 11 hours after the merger by the One- Meter, Two Hemisphere (1M2H) team using the 1 m Swope Telescope. The optical transient was independently detected by multiple teams within an hour. Subsequent observations targeted the object and its environment. Early ultraviolet observations revealed a blue transient that faded within 48 hours. Optical and infrared observations showed a redward evolution over ~10 days. Following early non-detections, X-ray and radio emission were discovered at the transientâs position ~9 and ~16 days, respectively, after the merger. Both the X-ray and radio emission likely arise from a physical process that is distinct from the one that generates the UV/optical/near-infrared emission. No ultra-high-energy gamma-rays and no neutrino candidates consistent with the source were found in follow-up searches. These observations support the hypothesis that GW170817 was produced by the merger of two neutron stars in NGC4993 followed by a short gamma-ray burst (GRB 170817A) and a kilonova/macronova powered by the radioactive decay of r-process nuclei synthesized in the ejecta
RNAcentral: a comprehensive database of non-coding RNA sequences
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- Basu S
- Bateman A
- Berardini TZ
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- Cannone JJ
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- Vlachos IS
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- Williams KP
- Wood V
- Wower J
- Yoshihama M
- Zhang Z
- Zhao Y
- Zhu W
- Zwieb CW
- Publication venue
- Nucleic Acids Research
- Publication date
- 28/10/2016
- Field of study
RNAcentral is a database of non-coding RNA (ncRNA) sequences that aggregates data from specialised ncRNA resources and provides a single entry point for accessing ncRNA sequences of all ncRNA types from all organisms. Since its launch in 2014, RNAcentral has integrated twelve new resources, taking the total number of collaborating database to 22, and began importing new types of data, such as modified nucleotides from MODOMICS and PDB. We created new species-specific identifiers that refer to unique RNA sequences within a context of single species. The website has been subject to continuous improvements focusing on text and sequence similarity searches as well as genome browsing functionality. All RNAcentral data is provided for free and is available for browsing, bulk downloads, and programmatic access at http://rnacentral.org/.Biotechnology and Biological Sciences Research Council (BBSRC) [BB/J019232/1]
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- Ălvarez ĂMC
- Ăvalos Y
- Ănal G
- ĂstĂŒn S
- ÄoliÄ M
- ÄokiÄ J
- Ćœerovnik E
- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2021
- Field of study
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field
Prevention of pertussis: An unresolved problem
- Publication venue
- 'Informa UK Limited'
- Publication date
- Field of study
A simple assay technique for pancreatic lipase
- Author
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Conservation Principles, and Environmental Transformation and Transport
- Author
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Comparative study of secretin and Lundh tests
- Author
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Augmenting the bootstrap to analyze high dimensional genomic data
- Author
- AP Gasch
- AR Kamat
- B Efron
- BW Silverman
- CR Rao
- D Angelis De
- DA Lashkari
- Francesca Chiaromonte
- IS Helland
- J SchÀfer
- J SchÀfer
- J Whittaker
- JM Cherry
- K Gunsalus
- KC Li
- L Breiman
- L Carrel
- L Carrel
- L Fernholz
- M Nei
- M Werner-Washburne
- MT Ross
- O Ledoit
- P Buhlmann
- P Hall
- RA Penrose
- RD Cook
- S Raudys
- Svitlana Tyekucheva
- T Hastie
- TI Lee
- TR Lezon
- Publication venue
- Publication date
- 01/01/2008
- Field of study
Inverse covariance, Large-p-small-n , Resampling, Genomics, 62G09, 62P10,
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