Contact information
Research groups
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.
Key publications
-
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
-
TBK1 and IKKε act like an OFF switch to limit NLRP3 inflammasome pathway activation.
Journal article
Fischer FA. et al, (2021), Proc natl acad sci u s a, 118
-
Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity.
Journal article
Boucher D. et al, (2018), J exp med, 215, 827 - 840
-
Sterile signals generate weaker and delayed macrophage NLRP3 inflammasome responses relative to microbial signals.
Journal article
Bezbradica JS. et al, (2017), Cell mol immunol, 14, 118 - 126
-
A role for the ITAM signaling module in specifying cytokine-receptor functions.
Journal article
Bezbradica JS. et al, (2014), Nat immunol, 15, 333 - 342
Recent publications
-
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
-
Activation of the Non-canonical Inflammasome in Mouse and Human Cells.
Journal article
Bezbradica JS. et al, (2022), Methods mol biol, 2459, 51 - 63
-
PHOrming the inflammasome: phosphorylation is a critical switch in inflammasome signalling.
Journal article
McKee CM. et al, (2021), Biochem soc trans, 49, 2495 - 2507
-
TBK1 and IKKε act like an OFF switch to limit NLRP3 inflammasome pathway activation.
Journal article
Fischer FA. et al, (2021), Proc natl acad sci u s a, 118
-
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.
Journal article
Klionsky DJ. et al, (2021), Autophagy, 17, 1 - 382