Conference Agenda

Overview and details of the sessions of this conference. Please select a date or location to show only sessions at that day or location. Please select a single session for detailed view (with abstracts and downloads if available).

 
 
Session Overview
Session
Session 4: Core Facility Session: Spectral Cytometry
Time:
Thursday, 01/Oct/2020:
3:30pm - 4:30pm

Session Chair: Frank Schildberg
Session Chair: Christian Kukat
Location: Zoom

Speakers: Simone Pöschel (Tübingen) and Bastian Höchst (München)


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Presentations

Implementing spectral cytometry in a core facility: one lab's experience with the Cytek Aurora

Simone Pöschel

Universitätsklinikum Tübingen, Germany

You want to take flow cytometry to the next level of performance?

The Cytec AURORA allows separation of fluorochromes with very close emission profiles by capturing the entire emission spectrum signature of the fluorescent dyes rather than just a section of it. This enables the use of a wide range of new fluorochrome combinations and opens the door to high complexity applications.

Having recently implemented the AURORA in our Core Facility, we would like to introduce you to this interesting technique and share our experiences of the establishing procedure. We will talk about advantages, challenges, pitfalls of technique and software and present first data and results.

Did we arouse your interest? We do look forward to exchanging our experiences with this powerful technique.



The metabolic momentum of MDSCs

Bastian Höchst

Technische Universität München, Germany

Myeloid derived suppressor cells (MDSCs) develop in the response to chronic inflammation and are key players in blunting immune responses against cancer. Despite the high importance of these cells in local regulation of effector T cells in cancer and intensive research efforts in this filed, no molecular marker has been identified that defines MDSCs.

We could show that MDSCs are characterized by a strongly reduced metabolism and that they transfer this hibernation-like state to CD8 T cells and thereby paralyze them.

This effect is caused by the accumulation of the dicarbonyl radical methylglyoxal, which is produced by the semicarbazide sensitive amine oxidase (SSAO). Methylglyoxal is transferred to the effector cells where it leads to a depletion of l-arginine.

In a preclinical model, we demonstrated that neutralization of methylglyoxal overcomes MDSC-mediated suppression and, in combination with checkpoint inhibition, leads to significantly improved cancer immunotherapy.

Our results identify methylglyoxal as a functional marker metabolite for MDSCs that mediates T-cell paralysis and may serve as a target for improving cancer immunotherapy.



 
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