e-learning
resources
Madrid 2019
Monday, 30.09.2019
Injury and repair: less is more
Login
Search all ERS
e-learning
resources
Disease Areas
Airways Diseases
Interstitial Lung Diseases
Respiratory Critical Care
Respiratory Infections
Paediatric Respiratory Diseases
Pulmonary Vascular Diseases
Sleep and Breathing Disorders
Thoracic Oncology
Events
International Congress
Courses
Webinars
Conferences
Research Seminars
Journal Clubs
Publications
Breathe
Monograph
ERJ
ERJ Open Research
ERR
European Lung White Book
Handbook Series
Guidelines
All ERS guidelines
e-learning
CME Online
Case reports
Short Videos
SpirXpert
Procedure Videos
CME tests
Reference Database of Respiratory Sounds
Radiology Image Challenge
Brief tobacco interventions
EU Projects
VALUE-Dx
ERN-LUNG
ECRAID
UNITE4TB
Disease Areas
Events
Publications
Guidelines
e-learning
EU Projects
Login
Search
The PD-1 immune checkpoint promotes lung damage in murine models of COPD-like inflammation
F. Ritzmann (Homburg, Germany), G. Vella (Homburg, Germany), A. Lis (Homburg, Germany), A. Angenendt (Homburg, Germany), C. Herr (Homburg, Germany), R. Bals (Homburg, Germany), C. Beisswenger (Homburg, Germany)
Source:
International Congress 2019 – Injury and repair: less is more
Session:
Injury and repair: less is more
Session type:
Oral Presentation
Number:
2120
Disease area:
Airway diseases
Rating:
You must
login
to grade this presentation.
Share or cite this content
Citations should be made in the following way:
F. Ritzmann (Homburg, Germany), G. Vella (Homburg, Germany), A. Lis (Homburg, Germany), A. Angenendt (Homburg, Germany), C. Herr (Homburg, Germany), R. Bals (Homburg, Germany), C. Beisswenger (Homburg, Germany). The PD-1 immune checkpoint promotes lung damage in murine models of COPD-like inflammation. 2120
You must
login
to share this Presentation/Article on Twitter, Facebook, LinkedIn or by email.
Member's Comments
No comment yet.
You must
Login
to comment this presentation.
Related content which might interest you:
Panel discussion on ERS Statement – A core outcome set for clinical trials evaluating the management of COPD exacerbations
ERS statement: a core outcome set for clinical trials evaluating the management of COPD exacerbations
Evidence-based eHealth for COPD
Related content which might interest you:
NTHi-induced inflammation activates the PD-1 immune checkpoint in the tumor microenvironment
Source: International Congress 2018 – Lung cancer: novel molecular markers and mechanisms
Year: 2018
IL-17A from innate and adaptive lymphocytes contributes to inflammation and damage in cystic fibrosis lung disease
Source: Eur Respir J, 57 (6) 1900716; 10.1183/13993003.00716-2019
Year: 2021
Tim-3 regulates Tregs’ ability to resolve the inflammation and proliferation of acute lung injury by polarizing M2c macrophages
Source: International Congress 2017 – Anti-inflammatory and pro-repair mediators in acute lung injury
Year: 2017
c-Met expression induction in immune cells modulates pulmonary fibrosis progression
Source: Virtual Congress 2020 – Physiological and cellular mechanisms affecting pulmonary pathologies
Year: 2020
Over-expression of SIGIRR attenuates TLR 4,5,9-mediated immune responses in human airway epithelial cells
Source: Annual Congress 2009 - Mechanisms of infection: what's new?
Year: 2009
The innate immune function of airway epithelial cells in inflammatory lung disease
Source: Eur Respir J 2015; 45: 1150-1162
Year: 2015
Galectin-9 attenuates acute lung injury in mice by inducing myeloid-derived suppressor cells
Source: Annual Congress 2010 - Emerging mechanisms in lung injury
Year: 2010
TD-0903, an inhaled JAK inhibitor in development for COVID-19, blocks ARDS-relevant hyperinflammation and lung injury in primary human immune and airway epithelial cells
Source: Virtual Congress 2021 – Emerging respiratory diseases: state-of-the-art studies of SARS-CoV-2 infection
Year: 2021
Impaired lung function is associated with systemic inflammation and macrophage activation
Source: Eur Respir J 2015; 45: 557-559
Year: 2015
Modulation of inflammatory cells apoptosis induced by oral tolerance in a model of chronic allergic airway inflammation in guinea pigs
Source: Annual Congress 2005 - Regulation of the allergic and asthmatic response
Year: 2005
Curcumin inhibits COPD-like airway inflammation and lung cancer promotion in mice
Source: Annual Congress 2009 - COPD and asthma - from the cell to the clinic
Year: 2009
Genetic deletion of SLPI promotes inflammatory cell recruitment in a model of chronic lung disease
Source: Virtual Congress 2021 – Emerging new mechanisms of chronic lung disease
Year: 2021
Gut microbial modulation attenuates emphysema development by suppressing inflammation and apoptosis
Source: Virtual Congress 2020 – New insight into the immunology of asthma and COPD
Year: 2020
Ghrelin ameliorates bleomycin-induced acute lung injury by protecting alveolar epithelial cells and suppressing lung inflammation
Source: Annual Congress 2012 - Fibrogenesis between epithelial injury and fibroblast proliferation
Year: 2012
The protective effects of SIGIRR on flagellin-induced acute inflammation of the airway in mice
Source: Annual Congress 2008 - Mechanisms of respiratory infections: interaction between the pathogen and the host
Year: 2008
IL-17R-deficient mice generate a Th2 response and altered leukocyte trafficking in a model of pulmonary inflammation
Source: Eur Respir J 2003; 22: Suppl. 45, 194s
Year: 2003
In vivo imaging of NF-kB pathway in acute lung inflammation mouse model can predict a pharmacological response
Source: Annual Congress 2011 - Cell biology of lung disease
Year: 2011
CD101 eosinophil serves as an early response to suppress endotoxin-induced acute lung injury
Source: International Congress 2018 – Role of microbial exposure and inflammation in lung injury
Year: 2018
Fas activation impairs the alveolar epithelial function in mice by mechanisms involving apoptosis
Source: Annual Congress 2011 - Anti-inflammatory strategies in acute lung injury
Year: 2011
IL-9 protects against bleomycin-induced lethal lung injury through a prostaglandin-dependent mechanism
Source: Eur Respir J 2004; 24: Suppl. 48, 105s
Year: 2004
We use cookies on our website to give you the most relevant experience by remembering your preferences and repeat visits. By clicking "Accept", you consent to the use of the cookies.
Accept