ANNUAL REVIEW master Final3a - St Vincent's University Hospital

targets for the rational development of novel therapies. Analysis of variations (polymorphisms) in the IFNα
and IFNα response genes and the resulting difference in response to interferon alpha may help us determine
patients who are most likely to respond to therapeutic interferon alpha.
Tariq Tajuddin, Emma McGrath, Elizabeth Ryan, John Hegarty, Cliona O’Farrelly.
Regulation of DC-SIGN by IFN-α
DC-SIGN is a C-type lectin receptor expressed by dendritic cells (DC) that binds to a HCV envelope protein.
DC-SIGN expression can be reduced following exposure to IFN-·. In this study we aim to determine the
importance of the expression of this receptor to the outcome of IFN-·/Ribavirin therapy.
Elizabeth Ryan, Cliona O’Farrelly, John Hegarty
The characterisation of T cell subsets in normal and diseased liver
T regulatory cells (CD4+CD25+FoxP3+) that secrete anti-inflammatory cytokines, such as IL-10 and TGFβ
can prevent effective cellular responses. By carefully characterising this population in normal and diseased
human liver tissue we aim to determine their importance in controlling the immune response in the liver.
Previous work in Prof. Kingston Mills’ Laboratory has shown that Fasciola hepatica infection of mice can
lessen the severity of Experimental Autoimmune Encephalitis (EAE). We aim to characterise liver T regulatory
cells in this model to determine their role in mediating the suppression of inflammation.
Eszter Nèmeth, Miriam Brady (TCD), Cliona O’Farrelly, Kingston Mills (TCD)
How does HCV inhibit Interferon-alpha (IFN-·) treatment?
A significant percentage of the Irish population are infected with HCV and IFN-· is the current standard
treatment. However, more than 50% of patients do not respond to this therapy and suffer significant side
effects unnecessarily. The anti-viral action of IFN-α depends on a cellular cascade of proteins known as the
JAK/STAT pathway. We are investigating how HCV affects this pathway and the subsequent anti-viral
response. Our initial results have discovered that a number of proteins of the JAK/STAT pathway are absent
in patients who fail to respond to therapy. We plan to determine how this virus destroys such important
proteins and in doing so we hope to provide clinicians with a predictive tool of response and identify potential
targets of for future therapy.
Nigel Stevenson, Catherine Keogh, Elizabeth Ryan, Tariq Tajuddin, John Hegarty, Cliona O’ Farrelly,
Aideen Long (TCD), Christine Biron (Brown University), Jim Johnston (Queen’s University, Belfast),
Charlie Rice (Rockefeller University)
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