Kerrilyn Diener

Biography

Robinson Research Institute Research Fellow Reproductive Immunology Group; Head, Prof Sarah Robertson: http://www.adelaide.edu.au/robinson-research-institute/researchers/group-leaders/robertson/ Projects: The effect of maternal anti-viral immune responses on reproductive success Viruses such as cytomegalovirus and Zika virus are known to affect fetal development. Dr Kerrilyn Diener, in collaboration with Prof Sarah Robertson and Prof John Hayball, are interested in understanding how the maternal immune response to such viral infections during pregnancy can impact on reproductive outcomes. Of particular interest is dissecting out how the maternal innate immune response can change immune and neurodevelopment in the fetus such that offspring exhibit altered immune responses and behavioural abnormalities upon further immune challenges after birth. The role of HMGB1, a damage-associated molecular pattern (DAMP), in neonatal sepsis Sepsis, an overwhelming infection, remains a leading cause of death in both adult and neonatal intensive care units, with preterm babies being particularly vulnerable to hospital-acquired infections. Dr Kerrilyn Diener, in collaboration with Prof John Hayball, A/Prof Michael Stark and Dr Nicki Hodyl are investigating how high-mobility box group 1 (HMGB1) potentiates disease. Building on previous studies performed with adult human samples and adult mouse models of disease, we aim to continue development of a passive antibody treatment for septic neonates that will increase survival and reduce the long term morbidity often observed in survivors of neonatal sepsis. The effect viral infection during the peri-conception period has on the induction of B regulatory cells Viral infections in humans have been linked to increased proportions of pregnancy complications including preeclampsia, preterm labour and miscarriage, although the mechanisms behind this are unclear. We have recently shown in mouse studies that a sub-clinical viral infection of the uterine tract during the pre-implantation period causes a dramatic reduction in local T regulatory cell numbers and results in decreased pregnancy rates and growth trajectories of resultant offspring. Over the past decade, investigations into a population of suppressor B cells, collectively known as regulatory B cells, have increased, particularly since studies of operationally tolerant (immunosuppression-free) kidney transplant recipients uncovered a molecular signature on the B cells that was different or absent in recipients with stable kidney function on immunosuppression or chronic rejection. Furthermore, evidence suggests that B cells are fundamental in sustaining T regulatory cells, with B cell-deficient mice also exhibiting a reduced frequency of T regulatory cells. One of the hallmarks of B regulatory cells is their capacity to produce IL-10, and in the abortion-prone murine model of pregnancy loss, a lack of CD19+CD5+CD1d+ regulatory IL-10 producing B cells is noted. Whilst within the reproductive field the study of B regulatory cells remains in its infancy, conclusions drawn from studies of other disease states suggests that an intimate relationship between B regulatory cells and T regulatory cells might be necessary for a robust and uneventful pregnancy.

Research Interest

Medicine,Medical Education,Research,etc