Contact information
Jelena Bezbradica Mirkovic
PhD
Professor of Immunology
I was a Career Development Fellow of the Kennedy Trust for Rheumatology Research (KTRR), and now I am a Professor of Immunology at the University of Oxford.
My research goal is to elucidate mechanisms that control the initiation and duration of inflammatory responses in innate immune cells. To accomplish this goal, we study innate sensing and signalling in myeloid cells, such as macrophages, as these cells typically initiate the inflammatory response. Our group investigates how innate cells integrate signals from cytokines (which report on infection or tissue injury) with signals from microbial and tissue-damage sensors to direct the most appropriate effector response.
The NLRP3 inflammasome is one such critical sensor of cell and tissue homeostasis that becomes activated in response to pathogen- or tissue-derived danger signals. While beneficial during infections and vaccinations, excessive and uncontrolled NLRP3 activity contributes to the development of several inherited diseases such as Cryopyrin-Associated Periodic Syndromes (CAPS), or acquired, non-communicable and lifestyle-related inflammatory diseases, such as Arthritis, Gout, or aging-associated inflammation and functional decline. Hence, we study how the NLRP3 pathway activity is ‘turned on and off’ in healthy individuals to be able to harness this knowledge for future therapeutic interventions allowing control over inflammasome response.
I earned my Ph.D. degree with Professor Sebastian Joyce at Vanderbilt University, USA. I continued my research training as a Damon Runyon Cancer Research Foundation and Howard Hughes Medical Institute postdoctoral fellow with Professor Ruslan Medzhitov at Yale University, USA, and with Professor Kate Schroder at The University of Queensland, Australia. I joined the Kennedy Institute in 2016.
Recent publications
Threat assessment shapes neutrophil cell fate upon inflammasome activation.
Journal article
Yow SJ. et al, (2026), Sci Adv, 12
BCG enables protection against malaria through adjuvanting an adenovirus-vectored vaccine.
Journal article
Reinke S. et al, (2026), NPJ Vaccines
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 following lytic cell death
Journal article
Jones Evana EL. et al, (2026), Science immunology
CLIC5 inhibitors developed with EVOTEC, academic team: Jelena Bezbradica Mirkovic, Christopher Buckley and Mark Coles to target CLIC5 in arthritis
Device/Product
BEZBRADICA MIRKOVIC J. et al, (2025)
Conditional CLIC5 KO in fibroblasts, new mouse model to study tissue damage in arthritis
Device/Product
BEZBRADICA MIRKOVIC J. et al, (2025)
CALHM6 deficient mouse to study role of ion channel CALHM6 in cell-cell interaction during inflammation
Device/Product
BEZBRADICA MIRKOVIC J., (2025)
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 MIRKOVIC J. and Bryant C., (2023), EMBO Reports