Research Program Immunology and Cancer - News & Notices

Kevin Bode: Dectin-1 binding to annexins on apoptotic cells induces peripheral immune tolerance via NADPH oxidase-2

Riccardo Pecori: RNA editing modulates pathways critical to B cell lymphomagenesis

"iReceptor plus: Federated Infrastructure for AIRR-seq Data"

"Using functional genetics to understand immune regulation in cancer"

"Panta rhei: Cellular flows in immune responses, hematopoiesis and leukemia"

Thesis Abstract: Our study revealed that SPTLC2 underpins the adaptive protective immunity by translating extracellular stimuli into intracellular anabolic signals and reducing the cellular stress in maintaining metabolic reprogramming sustainability. In addition, SPTLC2 is required to maintain the suppressive activity of Treg cells to keep the immune tolerance and restrict the anti-tumor responses. Collectively, we address that the SPTLC2-mediated sphingolipid de novo synthetic pathway synchronizes metabolic reprogramming and the immune reaction of regulatory and effector T cells in infection and cancer.

Abstract: T cell receptor (TCR) engagement and subsequent signalling are a prerequisite to initiate a T cell immune response. This study examined the role of Thioredoxin-interacting protein (TXNIP) in TCR signalling and shows that TXNIP acts as transcriptional inhibitor. Hence, TXNIP might be considered as a potential therapeutic target to shape T cell responses e.g. in autoimmune or tumour diseases.

Congratulations on this excellent work!

Abstract: My PhD work was focusing on the characteristic frameshift mutations of the Notch1 PEST domain, leading to the expression of a truncated, hyperactive Notch1 protein. These mutations are found with very high frequencies in human T-ALL, and also in our spontaneous T-ALL mouse model. To investigate the importance of such frameshift mutations in leukemia pathogenesis, we developed a modified Notch1 allele, where frameshift mutations are non-functional. Interestingly, mice bearing such a modified Notch1 allele overcome frameshift disability by specifically acquiring direct STOP mutations leading to a truncated PEST domain. Overall, our results reveal an enormous selection pressure for mutations leading to a hyperactive Notch signaling in T-ALL pathogenesis.

Congratulations Dr. Kongsaysak-Lengyel!

Abstract: In my PhD project I investigated the regulation of the hematopoietic system, and in particular HSC, under stress conditions. To enable HSC fate mapping, I employed a Cre knock-in reporter mouse and performed time-resolved analysis of hematopoietic compartment sizes and label propagation. Our findings show that the activation of HSC, in terms of differentiation, depends strongly on the nature of the challenge, giving important insights on the hematopoietic response to severe insults such as sepsis and irradiation.

Congratulations on this great work!