Professor Carola G Vinuesa



LMS(MBBS) (Madrid), PhD (Birmingham UK), Elizabeth Blackburn NHMRC Research Fellow


2017 News: See Professor Vinuesa's presentation at The World Economic Forum in Davos, Switzerland on 18 January 2017 here

Carola Vinuesa was born in Spain and obtained a medical degree at the University Autonoma of Madrid. She undertook specialist clinical training in the UK and in 2000 was awarded a PhD by the University of Birmingham. As the recipient of a Wellcome Trust International Travelling prize Fellowship, she did postdoctoral work at The John Curtin School for Medical Research (The Australian National University, ANU). Her work led to the discovery of genes important for immune regulation and memory and the identification of a novel pathway of posttranscriptional control of gene expression to prevent autoimmunity. Since 2006 she has been leading the Humoral Immunity and Autoimmunity Group at ANU, first supported by a Viertel Senior Medical Research Fellowship and currently by an Elizabeth Blackburn NHMRC Fellowship. Her group identified a critical role for follicular helper T (Tfh) cells in autoantibody-mediated autoimmune diseases and made significant discoveries into the function and transcriptional regulation of this cell subset. She has won several prizes including the 2008 Science Minister’s Prize (Life Scientist of the year), the 2009 Gottschalk Medal of the Australian Academy of Sciences, the inaugural CSL-Young Florey Medal and the 2015 Ramaciotti Medal for Excellence in Biomedical Research. In 2015 she was elected as a Fellow of the Australian Academy of Science. She is currently Professor of Immunology at the ANU. Since its launch in 2014, Carola has been joint Director of the Centre for Personalised Immunology (an NHMRC Centre of Research Excellence) that aims to dissect the genetic, molecular and cellular pathogenesis of immune disease in individual patients with the goal of improving diagnoses and identifying targeted therapies.




Research interests

We study how microRNA mediated regulation of gene expression in T follicular (TFH) helper cells, prevents the development of autoimmune diseases including lupus, type 1 diabetes and autoimmune arthritis. We take advantage of our discovery of the Roquin tolerance pathway to dissect the contribution of TFH cells and germinal centres to the development of pathogenic autoantibodies and TFH-cell derived lymphomas.  

Long-lasting antibody responses are a key component of the mammalian immune system; they protect us from the constant challenge of pathogenic bacteria and viruses. The quality of the antibodies that B cells produce matters: effective protection requires production of antibodies with high affinity. Affinity improvement occurs as a consequence of random mutation targeted at the genes that encode for the B cell receptor. Mutated B cells can be selected by a subset of T cells known as T follicular helper (Tfh) cells to become long-lived plasma cells that will secrete high affinity antibody for decades. However, this ability to produce long-lasting high affinity antibodies is a double-edged sword: perturbations can result in over 80 different autoimmune diseases that collectively affect 3-5 per cent of the population. These diseases include lupus, Type 1 diabetes, rheumatoid arthritis, and typically occur when the immune system cannot differentiate between invading pathogens and the body’s own cells, resulting in the destruction of tissues. Our research aims to understand autoimmune disease pathogenesis utilizing two different but complementary approaches. 


Updated:  23 January 2018/Responsible Officer:  Director, JCSMR/Page Contact:  Web Manager