Jelena Bezbradica Mirkovic

PhD

KTRR Senior Research Fellow

I am a Senior Research Fellow of the Kennedy Trust for Rheumatology Research (KTRR) at the University of Oxford.

My research focus is to understand innate immune responses to sterile versus microbe-induced tissue injury so that we can design therapies against inflammatory diseases caused by sterile injury without compromising the patient’s antimicrobial defences.

My group investigates how tissue resident immune cells such as macrophages integrate signals from cytokines (soluble mediators that report on tissue injury) with signals from microbial and tissue-damage sensors to direct a response that is best tailored to a specific pathophysiologic situation.

I earned my Ph.D. degree under the tutelage of 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 Doctor Kate Schroder at The University of Queensland, Australia. I joined the Kennedy Institute in 2016.

Key publications

Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity.
Journal article

Boucher D. et al, (2018), The Journal of experimental medicine, 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
Integration of cytokine and heterologous receptor signaling pathways.
Journal article

Bezbradica JS. and Medzhitov R., (2009), Nat Immunol, 10, 333 - 339
Granulocyte-macrophage colony-stimulating factor regulates effector differentiation of invariant natural killer T cells during thymic ontogeny.
Journal article

Bezbradica JS. et al, (2006), Immunity, 25, 487 - 497

Recent publications

Sterile signals generate weaker and delayed macrophage NLRP3 inflammasome responses relative to microbial signals
Conference paper

Coll RC. et al, (2018), EUROPEAN JOURNAL OF IMMUNOLOGY, 46, 850 - 850
STAYING ALIVE! SIGNAL PROCESSING BY NF-kappa B PROTECTS NKT CELLS FROM TNFR1-TRIGGERED DEATH
Conference paper

Kumar A. et al, (2018), JOURNAL OF IMMUNOLOGY, 200
Cutting Edge: Blockade of Inhibitor of Apoptosis Proteins Sensitizes Neutrophils to TNF- but Not Lipopolysaccharide-Mediated Cell Death and IL-1β Secretion.
Journal article

Chen KW. et al, (2018), Journal of immunology (Baltimore, Md. : 1950), 200, 3341 - 3346
Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity.
Journal article

Boucher D. et al, (2018), The Journal of experimental medicine, 215, 827 - 840
Interleukin-1β Maturation Triggers Its Relocation to the Plasma Membrane for Gasdermin-D-Dependent and -Independent Secretion
Journal article

Monteleone M. et al, (2018), Cell Reports

More publications