e-learning
resources
Paris 2018
Wednesday, 19.09.2018
Lung cancer: novel molecular markers and mechanisms
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
NTHi-induced inflammation activates the PD-1 immune checkpoint in the tumor microenvironment
F. Ritzmann (Homburg, Germany), G. Vella (Homburg, Germany), C. Herr (Homburg, Germany), R. Bals (Homburg, Germany), C. Beisswenger (Homburg, Germany)
Source:
International Congress 2018 – Lung cancer: novel molecular markers and mechanisms
Session:
Lung cancer: novel molecular markers and mechanisms
Session type:
Oral Presentation
Number:
5378
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), C. Herr (Homburg, Germany), R. Bals (Homburg, Germany), C. Beisswenger (Homburg, Germany). NTHi-induced inflammation activates the PD-1 immune checkpoint in the tumor microenvironment. 5378
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:
Combination therapy in the era of immunotherapy
Cisplatin/pemetrexed chemotherapy versus palliative care survival in malignant pleural mesothelioma
New pathways, new targets
Related content which might interest you:
The PD-1 immune checkpoint promotes lung damage in murine models of COPD-like inflammation
Source: International Congress 2019 – Injury and repair: less is more
Year: 2019
Inhibition of osteopontin modulates tumor-stimulated immune response and suppresses mesothelioma progression
Source: Annual Congress 2012 - Biology and treatment of malignant pleural effusions
Year: 2012
Central role for phosphoinositide-3-kinase gamma/delta dependent signalling in eosinophilic pulmonary inflammation driven by innate lymphoid cells
Source: International Congress 2017 – Therapeutic approaches in lung disease
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
IL-4 induces Th2 cells to resist the IL-27 counterregulation by downregulating STAT1 and STAT2 phosphorylation
Source: Annual Congress 2012 - Asthma: mechanisms of airway inflammation
Year: 2012
Nlrc5 is involved in allergic airway inflammation and negatively regulates inflammatory signaling pathway via TLR2/NF-?B.
Source: International Congress 2018 – Translational models of the immunopathology that underlies airway obstructive diseases
Year: 2018
A pathogen-activated innate homing pathway that instructs allergic inflammation
Source: Annual Congress 2007 - Regulation of allergic airway inflammation in animal models of asthma
Year: 2007
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
Stimulation of NOD1 induces RIP2, TAK1 and p38 MAPK dependent pro-inflammatory signalling in human lung microvascular endothelial cells
Source: Annual Congress 2011 - Mechanisms of acute lung injury and mesenchymal cell treatment
Year: 2011
Amifostine reduces lipopolysaccharide-induced lung dysfunction via suppression of redox-sensitive inflammatory signaling
Source: Annual Congress 2008 - Animal models of pulmonary fibrosis: mechanisms and therapies
Year: 2008
Inhibition of VEGF blocks the activation of TGF-β
1
through a PI3K/Akt signaling pathway in allergic airway disease of mice
Source: Annual Congress 2007 - Current issues in airway physiology, pharmacology and monitoring
Year: 2007
The role of innate immune cells in inflammation
Source: International Congress 2015 – Resolving inflammation
Year: 2015
ET-1 regulates pathological cell proliferation by ERK1/2 in a state of chronic inflammation
Source: Annual Congress 2010 - Novel cellular mechanisms in lung disease
Year: 2010
PPAR-gamma modulates allergic inflammation through upregulation of PTEN
Source: Eur Respir J 2005; 26: Suppl. 49, 25s
Year: 2005
A T cell-specific inhibitor of NF-kappaB and AP-1 suppresses lung fibrosis in mice
Source: Eur Respir J 2004; 24: Suppl. 48, 101s
Year: 2004
Decreased PTEN amplifies PI3K signaling and enhances pro-inflammatory cytokine release in COPD
Source: International Congress 2016 – Studies in airway cell biology
Year: 2016
Rhinovirus-induced proinflammatory cascade in bronchial epithelial cells requires xanthine-oxidase system activation
Source: Annual Congress 2008 - New diagnostic methods in viral and atypical infections
Year: 2008
The molecular mechanisms of lymphocyte apoptosis disregulation at Th1- and Th2- cytokine disbalance
Source: Annual Congress 2011 - Lung development and neoplasia
Year: 2011
GM-CSF and CSF-1 co-regulate lung inflammation and ERMP12
+
progenitor recruitment during immune responses to LPS
in vivo
Source: Eur Respir J 2006; 28: Suppl. 50, 300s
Year: 2006
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