- Cancer Immunotherapy and Biomarkers
- CAR-T cell therapy research
- Immune Cell Function and Interaction
- Immune Response and Inflammation
- T-cell and B-cell Immunology
- Psoriasis: Treatment and Pathogenesis
- Cell Adhesion Molecules Research
- Advanced Antenna and Metasurface Technologies
- Electromagnetic wave absorption materials
- Atherosclerosis and Cardiovascular Diseases
- Carbon and Quantum Dots Applications
- Immunotherapy and Immune Responses
Philipps University of Marburg
2020-2023
Abstract Intratumoral cytotoxic CD8+ T cells (CTL) enter a dysfunctional state characterized by expression of coinhibitory receptors, loss effector function, and changes in the transcriptional landscape. Even though several regulators T-cell exhaustion have been identified, molecular mechanisms inducing remain unclear. Here, we show that IL18 receptor (IL18R) signaling induces murine pancreatic cancer model. Adoptive transfer Il18r−/− OT-1 CTLs resulted enhanced rejection subcutaneous tumors...
<div>Abstract<p>Intratumoral cytotoxic CD8<sup>+</sup> T cells (CTL) enter a dysfunctional state characterized by expression of coinhibitory receptors, loss effector function, and changes in the transcriptional landscape. Even though several regulators T-cell exhaustion have been identified, molecular mechanisms inducing remain unclear. Here, we show that IL18 receptor (IL18R) signaling induces murine pancreatic cancer model. Adoptive transfer...
<p>Supplementary Table S1-3 and Figures S1-6</p>
<div>Abstract<p>Intratumoral cytotoxic CD8<sup>+</sup> T cells (CTL) enter a dysfunctional state characterized by expression of coinhibitory receptors, loss effector function, and changes in the transcriptional landscape. Even though several regulators T-cell exhaustion have been identified, molecular mechanisms inducing remain unclear. Here, we show that IL18 receptor (IL18R) signaling induces murine pancreatic cancer model. Adoptive transfer...
<p>Supplementary Table S1-3 and Figures S1-6</p>
<div>Abstract<p>Intratumoral cytotoxic CD8<sup>+</sup> T cells (CTL) enter a dysfunctional state characterized by expression of coinhibitory receptors, loss effector function, and changes in the transcriptional landscape. Even though several regulators T-cell exhaustion have been identified, molecular mechanisms inducing remain unclear. Here, we show that IL18 receptor (IL18R) signaling induces murine pancreatic cancer model. Adoptive transfer...
<p>Supplementary Table S1-3 and Figures S1-6</p>
<p>Supplementary Table S1-3 and Figures S1-6</p>
Einleitung Durch Multiphotonenmikroskopie (MPM) können dreidimensionale Bilder von komplexen Geweben erzeugt werden. So ist die mikroskopische Untersuchung intratumoralen T-Zellen in vivo/in situ möglich. Intratumorale sind durch einen Verlust der Effektorfunktion gekennzeichnet, ein Phänomen, das als Exhaustion bekannt ist. In unserem Projekt werden CD8+ zytotoxische (CTL) auf Nlrp3/IL-18/IL-1β-vermittelte Mechanismen T-zellulären Dysfunktion untersucht.
Einleitung In duktale Adenokarzinome des Pankreas infiltrierende CD8+ zytotoxische T-Zellen (CTL) zeigen reduzierte Effektorfunktionen; dieser dysfunktionale Zustand wird T cell exhaustion genannt. Die proinfammatorischen Zytokine IL-1β und IL-18 spielen bei der Differenzierung von CTL eine wichtige Rolle. Deren Effektorfunktion über Antigen-abhängige Kontakte mit Zielzellen vermittelt; daher ist das Migrations- Interaktionsverhalten intratumoraler entscheidend für die Tumorimmunabwehr.