Pathometabolism of Myeloid Cells

Methodology:
We combine a variety of immunologic and metabolic methods to understand the phenotypic changes and mechanistic actions triggered by disease conditions-associated metabolites. Notably, mass spectrometry will be the central methodology contributing to studies in not only our group, but also the whole department (Head: Prof. Dr. Karsten Hiller). We utilize targeted and non-targeted metabolomics to discover potential metabolites, and apply stable isotopomers-assisted flux analysis to uncover metabolic pathways. Disease models will be implemented with in vitro cell-based studies and in vivo mouse studies (in strong collaborations with national and international partners).

Teaching for master students: SB23, Pathologic metabolism in human diseases – focusing on immune cells.

Master thesis: role of key metabolites in macrophage metabolism and function - in the context of diseases.
If you are interested, don't hesitate to contact.

News: Itaconate aggravates immunopathology via the CXCL10–CD8 T cell axis – our new study published in Exp Mol Med. 2026 Jun 5.

In our last study, we identified itaconate (and its isomer mesaconate) as immunosuppressive agent against LPS-stimulated IL-6 and IL-12 in macrophages. Interestingly, we also noticed that some factors were upregulated by itaconate. Due to limitations in disease models, we didn’t move on to explore the potential pathologic role of itaconate via these up-regulated factors.

Coincidentally, in a Cell Symposium in 2023, I met Dr. Junna Ye and Dr. Yue Sun from Ruijin Hospital, Shanghai Jiaotong University. They found out a correlation between itaconate and the Still’s Disease, a serious autoinflammatory disease and they had demonstrated a pathogenic role of itaconate in this disease, in contrast to the reported anti-inflammatory role of itaconate. Upon re-visiting my discovered itaconate-triggered chemokines, I suggested CXCL10 as a potential mediator of the pathogenic role of itaconate. With extensive analysis of patient samples, animal studies and cell culture experiments, we worked together to exhibit a myeloid-CD8 T cell crosstalk mediated by an itaconate-CXCL10 axis, triggering hepatic pathology in Still’s Disease, in parallel to the anti-inflammatory effects of itaconate on canonical cytokines. Therefore, this study reveals itaconate as a dual regulator in inflammatory diseases, where spatiotemporal context might dictate its efficacy – either anti-inflammatory or pro-pathologic.