Dr Amy Saunders

Amy Saunders – Research summary

Dr Amy Saunders

Dr Amy Saunders

The current research in my lab studies tolerogenic signals between epithelial cells and innate immune cells in the skin. The main function of the skin is to act as a barrier between the external environment and the internal body systems. Therefore this organ contains a plethora of immune cells poised to respond to invading pathogens. However, the skin is also colonised by beneficial commensal microbes which the immune system must remain tolerant to, in order to avoid inappropriate inflammation.

Psoriasis is a prevalent inflammatory skin disease which is triggered in predisposed individuals by stimuli such as stress, infection, injury, environmental triggers, or changes in the microbiota.

I am studying pathways which actively maintain the insensitivity of innate immune cells to innocuous stimuli under homeostatic conditions. Pathways such as these have been shown to be important in other organs such as the lung, and it is our hypothesis that these signals may be dysregulated in individuals suffering from inflammatory skin diseases such as psoriasis. I am, therefore, investigating the role of these pathways in psoriasis and determining if they hold novel therapeutic targets for the treatment of this disease.

Email: amy.saunders@manchester.ac.uk Tel: 0161 275 1690

Publications

  • Pauline Johnson, Asanga Samarakoon, Amy E. Saunders and Kenneth W. Harder. 2012. Encyclopedia of Signalling Molecules.
  • Bernhard, W., K. Barreto, A. Saunders, M. S. Dahabieh, P. Johnson, and I. Sadowski. 2011. The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response. FEBS letters 585:3549-3554.
  • Saunders, A. E., and P. Johnson. 2010. Modulation of immune cell signalling by the leukocyte common tyrosine phosphatase, CD45. Cellular signalling 22:339-348
  • Saunders, A., L. M. Webb, M. L. Janas, A. Hutchings, J. Pascall, C. Carter, N. Pugh, G. Morgan, M. Turner, and G. W. Butcher. 2010. Putative GTPase GIMAP1 is critical for the development of mature B and T lymphocytes. Blood 115:3249-3257.
  • Wong, V. W., A. E. Saunders, A. Hutchings, J. C. Pascall, C. Carter, N. A. Bright, S. A. Walker, N. T. Ktistakis, and G. W. Butcher. 2010. The autoimmunity-related GIMAP5 GTPase is a lysosome-associated protein. Self/nonself 1:259-268.
  • Barnes, M. J., H. Aksoylar, P. Krebs, T. Bourdeau, C. N. Arnold, Y. Xia, K. Khovananth, I. Engel, S. Sovath, K. Lampe, E. Laws, A. Saunders, G. W. Butcher, M. Kronenberg, K. Steinbrecher, D. Hildeman, H. L. Grimes, B. Beutler, and K. Hoebe. 2010. Loss of T cell and B cell quiescence precedes the onset of microbial flora-dependent wasting disease and intestinal inflammation in Gimap5-deficient mice. J Immunol 184:3743-3754.
  • Saunders, A., T. Lamb, J. Pascall, A. Hutchings, C. Dion, C. Carter, L. Hepburn, J. Langhorne, and G. W. Butcher. 2009. Expression of GIMAP1, a GTPase of the immunity-associated protein family, is not up-regulated in malaria. Malaria journal 8:53.

Publications

  • Pauline Johnson, Asanga Samarakoon, Amy E. Saunders and Kenneth W. Harder. 2012. Encyclopedia of Signalling Molecules.
  • Bernhard, W., K. Barreto, A. Saunders, M. S. Dahabieh, P. Johnson, and I. Sadowski. 2011. The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response. FEBS letters 585:3549-3554.
  • Saunders, A. E., and P. Johnson. 2010. Modulation of immune cell signalling by the leukocyte common tyrosine phosphatase, CD45. Cellular signalling 22:339-348
  • Saunders, A., L. M. Webb, M. L. Janas, A. Hutchings, J. Pascall, C. Carter, N. Pugh, G. Morgan, M. Turner, and G. W. Butcher. 2010. Putative GTPase GIMAP1 is critical for the development of mature B and T lymphocytes. Blood 115:3249-3257.
  • Wong, V. W., A. E. Saunders, A. Hutchings, J. C. Pascall, C. Carter, N. A. Bright, S. A. Walker, N. T. Ktistakis, and G. W. Butcher. 2010. The autoimmunity-related GIMAP5 GTPase is a lysosome-associated protein. Self/nonself 1:259-268.
  • Barnes, M. J., H. Aksoylar, P. Krebs, T. Bourdeau, C. N. Arnold, Y. Xia, K. Khovananth, I. Engel, S. Sovath, K. Lampe, E. Laws, A. Saunders, G. W. Butcher, M. Kronenberg, K. Steinbrecher, D. Hildeman, H. L. Grimes, B. Beutler, and K. Hoebe. 2010. Loss of T cell and B cell quiescence precedes the onset of microbial flora-dependent wasting disease and intestinal inflammation in Gimap5-deficient mice. J Immunol 184:3743-3754.
  • Saunders, A., T. Lamb, J. Pascall, A. Hutchings, C. Dion, C. Carter, L. Hepburn, J. Langhorne, and G. W. Butcher. 2009. Expression of GIMAP1, a GTPase of the immunity-associated protein family, is not up-regulated in malaria. Malaria journal 8:53.

Collaborators

Professor Tracy Hussell
Professor Chris Griffiths

Biography

I received a BSc in Biochemistry from the University of Warwick and briefly worked at AstraZeneca as a Summer Student in the Respiratory and Inflammatory research area. I then moved to the Babraham Institute at the University of Cambridge where I did a PhD with Geoff Butcher studying the role of the small GTPase, GIMAP1, in lymphocytes. During this project I also worked with Jean Langhorne at the NIMR, Mill Hill, investigating the role of GIMAP1 in malaria. For my postdoc I moved to the University of British Columbia in Vancouver, Canada where I was in Pauline Johnson’s lab studying the role of CD45 in innate immune cells. At the end of 2012 I moved to Manchester as a Postdoctoral Research Fellow.