Selected publications

• Gutowska-Owsiak D, Schaupp AL, Salimi M, Taylor S, and Ogg GS (2011) IL-22 down-regulates filaggrin expression and effects expression of profilaggrin processing enzymes. Br J Dermatol, 12(165):492-8.

• Aslam Aamir, Chan Hsien, Warrell David A, Misbah Siraj, and Ogg Graham S (2010) Tracking antigen-specific T-cells during clinical tolerance induction in humans. PLoS One, 5(6):e11028.

• Malavige Gathsaurie N, Jones Louise, Kamaladasa S D, Wijewickrama A, Seneviratne S L, Black Antony P, and Ogg Graham S (2008) Viral load, clinical disease severity and cellular immune responses in primary varicella zoster virus infection in Sri Lanka. PLoS One, 3(11):e3789.

• Black Antony PB, Ardern-Jones Michael R, Kasprowicz Victoria, Bowness Paul, Jones Louise, Bailey Abigail S, and Ogg Graham S (2007) Human keratinocyte induction of rapid effector function in antigen-specific memory CD4+ and CD8+ T cells. Eur J Immunol, 37(6):1485-93.

Graham Ogg

Skin and mucosae frequently represent the first point of contact with pathogens and allergens, yet we still know relatively little of the role of the surface immune system in clearing such challenges. This is crucially important in understanding the mechanisms of skin diseases and related diseases, and for optimising approaches to cutaneous drug and vaccine delivery.  The aim of the group is therefore to understand the role of human cutaneous cellular immune system in disease, treatment and vaccination.  We are investigating this aim through studies based on two common human diseases, atopic eczema and varicella zoster virus infection.

Atopic eczema is a very common problem which carries an enormous burden on patients and their families.  We know that skin barrier impairment is an important component of the disease, but it is not clear how this leads to inflammation and how in turn, the inflammation can contribute to further barrier compromise and to clinical disease.  It is important to answer these questions, in order to appropriately use existing medications and to develop new ones.

We have shown that common infections of the skin worsen the inflammation that can follow allergen exposure, and have progressed our understanding of the key cells and molecules that are involved.  We are now using this information to undertake clinical trials of new approaches to treatment and prevention.