Steve Anderton's group studies the initiation and resolution of T cell-mediated immunopathologies (chiefly autoimmune and allergic pathologies), with the aim of developing more effective/specific immunotherapies.
Our main research focus is on the signals that lead to the activation of T cells that cause autoimmune and allergic pathology. This has direct clinical relevance to understanding how the therapeutic use of antigenic peptides can switch-off the T cells that drive autoimmune and allergic diseases. The lab also works on the roles of B cells and of Foxp3+ regulatory T cells in the natural resolution of CNS autoimmune disease, and on how these cells interact with pathogenic effector T cells. This is also now being explored in the context of allergic inflammation in the lung.
Autoimmune and allergic diseases develop because of unwanted activation of CD4+ T lymphocytes in response to self proteins ("auto-antigens") or harmless environmental antigens. The complex processes of immune tolerance are designed to prevent this from happening. Our interests are in understanding how immune tolerance can break down and how it might be restored therapeutically in these diseases. To achieve this, our current research questions can be summarized as follows:-
a) what are the interactions between T cells and APC that determine the size and quality of the T cell response to antigen?
b) what are the key T cell functions that drive autoimmune and allergic disease?
c) what are the key regulatory functions and cellular interactions that can reverse ongoing immunopathology?
d) what are the rules that determine how effector and memory T cells respond to the therapeutic administration of antigen peptide in tolerogenic form?
Steve Anderton received his PhD from the University of Newcastle (1991), before moving to the University of Utrecht, The Netherlands, with a Wellcome Trust fellowship. This work asked how T cell responses to bacterial heat shock proteins could protect against experimental autoimmune arthritis and was one of the first studies to suggest that provoking a T cell response against a self-antigen could actually be beneficial - as long as it was the right type of (regulatory) T cell response. This triggered Steve’s continuing interest in antigen-based immunotherapy and he moved to work with David Wraith on peptide-based therapy of autoimmune disease (initially at Cambridge University and then Bristol University). Steve established his own group in Edinburgh in 2000, supported by successive MRC fellowships (Career Development Fellowship and Senior Research Fellowship). Steve joined CIR in 2008 with an RCUK Fellowship in Translational Medicine. He was appointed to a personal chair in Therapeutic Immunology in 2007.