Contact information
Jelena Bezbradica Mirkovic
PhD
Professor of Immunology
I am Professor of Immunology at the University of Oxford and was previously a Career Development Fellow of the Kennedy Trust for Rheumatology Research (KTRR).
My research seeks to understand how macrophages use inflammasomes, inflammatory cell death, and intercellular communication to sense tissue damage and shape sterile inflammation. Using molecular, cellular, and in vivo approaches, we investigate how innate immune sensing pathways enable macrophages to detect tissue damage and coordinate inflammatory responses within tissues.
A major focus of our work is the NLRP3 inflammasome, a key regulator of sterile inflammation implicated in a wide range of inflammatory and age-associated diseases. We study how inflammasome activity and inflammatory cell death are regulated within tissues, and how these pathways contribute to tissue pathology and chronic inflammatory disease.
More recently, we have become interested in understanding how macrophages communicate inflammatory information to neighbouring cells. This work includes studies of CALHM6-dependent ATP signalling and other emerging mechanisms of intercellular communication that coordinate tissue-level inflammatory responses.
I obtained my PhD with Professor Sebastian Joyce at Vanderbilt University. I subsequently trained as a Damon Runyon Cancer Research Foundation and Howard Hughes Medical Institute postdoctoral fellow with Professor Ruslan Medzhitov at Yale University and with Professor Kate Schroder at The University of Queensland before joining the Kennedy Institute of Rheumatology in 2016.
Recent publications
Salmonella effector SteE reprograms the macrophage regulatory network to drive specific hyperactivation of STAT3 target genes.
Journal article
Diaz-Del-Olmo I. et al, (2026), Mol Cell
TANK-binding kinase 1 (TBK1): unexpected cell type-specific immune regulation beyond antiviral type I interferon signaling.
Journal article
Almeida MS. et al, (2026), Curr Opin Virol, 76
The autoantigen TRIM21 assembles proinflammatory immune complexes after lytic cell death.
Journal article
Jones Evans EL. et al, (2026), Sci Immunol, 11
TBK1 and IKKε prevent premature cell death by limiting the activity of both RIPK1 and NLRP3 death pathways.
Journal article
Fischer FA. et al, (2025), Sci Adv, 11
Inflammasomes as regulators of mechano-immunity.
Journal article
Bezbradica JS. and Bryant CE., (2024), EMBO Rep, 25, 21 - 30
Emulsion and liposome-based adjuvanted R21 vaccine formulations mediate protection against malaria through distinct immune mechanisms.
Journal article
Reinke S. et al, (2023), Cell Rep Med, 4
The ion channel CALHM6 controls bacterial infection-induced cellular cross-talk at the immunological synapse.
Journal article
Danielli S. et al, (2023), EMBO J, 42
How Pyroptosis Contributes to Inflammation and Fibroblast-Macrophage Cross-Talk in Rheumatoid Arthritis.
Journal article
Demarco B. et al, (2022), Cells, 11
B cell-intrinsic TBK1 is essential for germinal center formation during infection and vaccination in mice.
Journal article
Lee MSJ. et al, (2022), J Exp Med, 219
ctivation of the Non-canonical Inflammasome in Mouse and Human Cells.
Journal article
Bezbradica JS. et al, (2022), Methods Mol Biol, 2459, 51 - 63