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Dr Lindsay Nicholson


I graduated from Cardiff Medical School and after training as a physician went to King’s College London to complete a PhD studying thyroid autoimmunity (or Grave’s disease), with Paul Banga and Alan McGregor. During my time as a PhD student, I developed a longstanding interest in the mechanisms of T cell recognition and activation. For anyone interested in autoimmune disease, this issue of how pathogenic cells get activated is key.

Trying to answer this question took me from London to Boston, to Vijay Kuchroo’s laboratory. Here we focussed on how peptides with single amino acid substitutions (altered peptide ligands) influence the type of autoimmune response that in people causes multiple sclerosis. Quite early in my time with Vijay, we published a paper in this area, showing that altered peptide ligands (APLs) could modulate experimental autoimmune encephalomyelitis (Immunity 3: 397-405 1995). In work with Ana Anderson, we found that certain MHC molecules could be associated with large populations of autoantigen specific T cells (Journal Of Experimental Medicine 191:761-770 2000). This led us to a novel hypothesis that explained the well known association between specific MHC haplotypes and autoimmune disease; specifically that some MHC molecules selected a more potentially dangerous repertoire of T cells than others. I also continued to work on cross-reactive T cell responses. Much of this work was covered in a review that Vijay, other members of his lab and I wrote (Annual Review of Immunology 20:101-123 2002).

In 2003 I moved to Bristol University where I extended my interest in organ specific autoimmune disease to the eye. The work in my lab in Bristol continues my long term interest in how autoimmune inflammation is initiated and regulated. We have made significant progress in characterising and monitoring models of clinical disease and have focussed in part on macrophage dependent regulation of the immune response within the target organ. I have also collaborated in developing various quantitative models of autoimmunity. Our main goal remains to control autoimmune inflammation safely and specifically, to treat the chronic debilitating conditions it causes.