Nadja Leinung, PhD

Postdoc

The enzyme IL4I1 (Interleukin-4 Induced 1) is a secreted L-amino acid oxidase producing metabolites with immunomodulatory functions. Beyond its established role in immune regulation, IL4I1 has emerged as a potential modulator of ferroptosis. Ferroptosis is not an isolated event — it can trigger necroinflammation, a state where cell death itself drives immune activation. Cells undergoing necrotic cell death release damage-associated molecular patterns (DAMPs), inducing the secretion of pro-inflammatory cytokines, which can further propagate cell death pathways, including necroptosis and pyroptosis.

Is IL4I1 exclusively an immune regulator, or does it also play a role in non-immune cells? Could IL4I1 represent an intrinsic cellular defense mechanism against ferroptosis, and if so, under what physiological or pathological conditions does this protection become relevant?

This project aims to uncover how IL4I1 influences ferroptosis and necroinflammation, shaping the interplay between different cell death mechanisms, and also cell death propagation.

Research interest:

• Ferroptosis

• Antioxidant balance

• Diabetic nephropathy