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You are here: FRIAS Fellows Fellows 2019/20 Prof. Dr. Cecile King

Prof. Dr. Cecile King

The Garvan Institute for Medical Research/St. Vincent’s Clinical School, UNSW Medicine
Immunology
External Senior Fellow
Marie S. Curie FCFP Fellow
September - January 2019

Room 01 024
Phone +49 (0) 761-203 97355
Fax +49 (0) 761-203 97451

CV

Dr King received her PhD from the Institute for Child Health Research, University of Western Australia and completed her postdoctoral training at the Scripps Research Institute, La Jolla, USA. Dr King joined the faculty of the Department of Immunology at the Garvan Institute for Medical Research, Sydney, Australia in 2005 and is a conjunct Associate Professor at the Department of Medicine, University of New South Wales.

Dr King continues to be intrigued by how the immune system maintains tolerance to self. Her research is focused on how interactions between the environment and immune system influence chronic inflammation and autoimmune disease. Dr King has made some important contributions to our understanding of how cytokines influence adaptive immune responses, including the identification of IL-21 as a therapeutic target in autoimmune disease. Dr King’s interests now include genes within type 1 IFN regulatory pathways that are associated with autoimmune disease risk and how these innate immune genes influence adaptive immune responses.

Selected Publications

  • Claudia Loetsch, Joanna Warren, Christoph Jandl, Adrienne Laskowski, David Thorburn, David Ryugo, Jonathan Sprent, Marcel Batten and Cecile King (2017). Cytosolic recognition of RNA drives the immune response to heterologous erythrocytes. Cell Reports Nov 7;21(6):1624-1638. doi: 10.1016/ j.celrep.2017.10.044.
  • Christoph Jandl, Sue M. Liu, Pablo F. Cañete, Joanna Warren, William E. Hughes, Alexis Vogelzang, Kylie Webster, Maria E. Craig, Gulbu Uzel, Alexander Dent, Polina Stepensky, Bärbel Keller, Klaus Warnatz, Jonathan Sprent and Cecile King (2017). IL-21 restricts regulatory T cells through Bcl-6 mediated inhibition of responsiveness to IL-2. Nature Communications Mar 17;8:14647. doi: 10.1038/ncomms14647.
  • Helen McGuire, Alexis Vogelzang, Cindy S Ma, William E. Hughes, Pablo Silveira, Stuart G Tangye, David Fulcher, Daniel Christ, Marika Falcone and Cecile King (2011). A Subset of Interleukin-21(+) Chemokine Receptor CCR9(+) T Helper Cells Target Accessory Organs of the Digestive System in Autoimmunity. Immunity, 2011 Apr 22;34(4):602-15.
  • Alexis Vogelzang, Helen M. McGuire, Jon Sprent Charles R. Mackay and Cecile King (2008). A fundamental role for IL-21 in T helper cell differentiation. Immunity, Jul;29(1):127-37.

FRIAS Research Project

Interleukin-21 induced formation of STAT1 and STAT3 dimers.

Our bodies rely on the production of antibodies to fight infection. In simple terms, our immune system contains B cells, which make antibodies, T cells, which help them and chemical messengers known as ‘cytokines’ that modulate this process. The cytokine IL-21 is produced by specialised cells known as T follicular helper cells, which help select B cells that produce the most potent antibodies. When IL-21 binds to its receptor (IL-21R) on the surface of a cell, it activates signals inside the cell to influence its behaviour, namely the Jak/STAT signalling pathway- through the phosphorylation of the proteins STAT1 and STAT3. We have generated a novel mouse that contains a single mutation in the IL-21R (Il21rEINS) that diminishes STAT1 activation, with no effect on STAT3. This minor genetic lesion had the fascinating outcome of dampening down the immune response. HYPOTHESES: IL-21 induces the activation of STAT1 and STAT3 proteins that form hetero- and homodimers that impart their functions on cell fate by binding to DNA and influencing gene transcription. We hypothesise that the formation of STAT dimers is influenced by the relative abundance of different forms of activated STAT proteins. RESEARCH PLAN: We will take advantage of Signalling and Immunological expertise at Freiburg University to analyse the formation of STAT dimers in the context of IL-21:IL-21 signalling in human cells with mutations in STAT signalling.