We are a systems immunology laboratory in the Department of Internal Medicine 3 – Rheumatology and Immunology at Erlangen University Hospital.
Our group investigates the mechanisms driving immune cell heterogeneity in tissues and inflammatory conditions and the links to disease variation across individuals. Our approach is characterized by a combination of high dimensional discovery in patient samples (in particular in the context of innovative therapies such as CAR-T cells) with in vitro systems, CRISPR-mediated genetic perturbations and murine models. We also develop novel analysis tools for high dimensional data.
In published work, we demonstrated that neutrophils in homeostasis are organized a chronologically ordered main sequence, termed neutrotime. In experimental inflammation, neutrophils reach distinct polarization states driven by timepoint, tissue and stimulus.
To apply this principle to human immune-mediated disease, we developed a method to jointly analyze murine and human transcriptomic data. Thereby, we identified a transcriptional program which characterizes neutrophils in the arthritic joint in both mice and humans. Functionally, this program was highly enriched for interferon gamma response genes, which we validated on the protein level and using in vitro models.
IZKF-N10 LAMP1 in Lupus Nephritis: LAMP1+ neutrophils in lupus nephritis
My preliminary data highlight that neutrophil phenotypes define distinct SLE patients and that LAMP-1 is a strongly dysregulated protein in SLE. I hypothesize that LAMP1 expression defines a distinct activation state of neutrophils associated with a clinical subgroup of SLE patients with more severe kidney involvement. Hence, this project aims to study the functional role of LAMP1 in neutrophils and probe associations of LAMP1 expression and serum levels with clinical features in SLE.
We are a systems immunology laboratory in the Department of Internal Medicine 3 – Rheumatology and Immunology at Erlangen University Hospital.
Our group investigates the mechanisms driving immune cell heterogeneity in tissues and inflammatory conditions and the links to disease variation across individuals. Our approach is characterized by a combination of high dimensional discovery in patient samples (in particular in the context of innovative therapies such as CAR-T cells) with in vitro systems, CRISPR-mediated genetic perturbations and murine models. We also develop novel analysis tools for high dimensional data.
In published work, we demonstrated that neutrophils in homeostasis are organized a chronologically ordered main sequence, termed neutrotime. In experimental inflammation, neutrophils reach distinct polarization states driven by timepoint, tissue and stimulus.
To apply this principle to human immune-mediated disease, we developed a method to jointly analyze murine and human transcriptomic data. Thereby, we identified a transcriptional program which characterizes neutrophils in the arthritic joint in both mice and humans. Functionally, this program was highly enriched for interferon gamma response genes, which we validated on the protein level and using in vitro models.
IZKF-N10 LAMP1 in Lupus Nephritis: LAMP1+ neutrophils in lupus nephritis
(FAU Funds)
2024
2023
2022
2021
2020
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