Name Professor Graham Ogg FRCP Dphil Bmbch BA


Curriculum Vitae

Personal Details

Name Professor Graham Ogg FRCP DPhil BMBCh BA

Nationality UK


Present Positions

1st October 2010- Professor of Dermatology, University of Oxford

1st October 2008- MRC Programme Leader, Human Immunology Unit

1st April 2008- Clinical Lead Dermatology Thames Valley and S Midlands LCRN (previously Chairman Dermatology Thames Valley CLRN)

1st April 2007- Sub-theme leader Biomedical Research centre and NIHR Investigator

1st October 2003- Associate Senior Research Fellow, Christ Church, Oxford

31st December 2001- Consultant Dermatologist, Oxford

Previous Positions

31st March 2003-8 MRC Senior Clinical Fellow, University of Oxford

9th April 2006-9 Chairman British Society for Investigative Dermatology

1st September 2006-9 Co-Editor of Clinical and Experimental Dermatology journal

MRC Clinician Scientist Fellow (1.10.98-31.3.03) and Specialist Registrar in Dermatology, Oxford Region (NTN OXF/005/008 1.1.98-31.12.01) and Junior Research Fellow, Christ Church (1.10.99-30.9.03)

MRC Clinical Training Fellow (1.1.96-30.9.98), Honorary Registrar in Dermatology, Churchill Hospital, Oxford (1.1.96-31.12.97), Clinical Lecturer, Magdalen College (1.10.98-30.9.99), and Senior Scholar Keble College (1.9.96-1.9.98).

SHO St John's Institute of Dermatology, Guy's Hospital, London (1.4.95-30.9.95) - SHO experience in dermatology (Prof R Hay, Dr JNWN Barker, Dr MacDonald), general medicine, GU and HIV.

SHO Royal Brompton Hospital, London (1.8.94-31.1.95) - SHO experience in cardiology (Dr Oldershaw and Prof Poole-Wilson) and ITU (Dr Evans).

SHO Hammersmith Hospital, London (1.2.94-31.7.94) - SHO experience in general medicine, respiratory medicine (Prof Pride), infectious disease (Prof Cohen), and renal medicine (Prof Rees).

SHO National Hospital for Neurology, Queen Square, London (1.8.93-31.1.94) - SHO experience under Profs Marsden, Harding, Frackowiak, Thomas.

Research Achievements

I have been fascinated by the cellular immune system since my undergraduate project in 1989 under the supervision of Professor Andrew McMichael. During my subsequent DPhil in Professor McMichael’s laboratory, I was part of an exciting group and shared in the achievements of the team. This included the first application of the use of HLA tetrameric complexes to questions relevant to disease pathogenesis (HIV) and the identification of CD94 as being a ligand for HLA-E. I wanted to apply my T cell knowledge to the understanding of human skin disease, as dermatology is my clinical speciality. One of the earliest achievements was working with Professor Vincenzo Cerundolo in which we showed that individuals with vitiligo have high frequencies of circulating melanocyte-specific T cells – this has been confirmed in many subsequent studies by others, and a potential role of such T cells in disease has been suggested by the acquisition of pigment loss in patients with melanoma treated with melanocyte-specific T cell infusions. Since having my own group under the support of an MRC Senior Clinical Fellowship, I have focused on atopic skin disease. We have made several contributions, including the identification of type 2 innate lymphoid cells (ILC2) in the skin of humans, and a further infiltration in eczematous lesions and after allergen challenge. We have defined cytokine and lipid mediators that promote ILC2 activation, with therapeutic implications which we are investigating in a current clinical trial. More recently, in collaboration with Professor Cerundolo, we have found that allergens generate neolipids which are novel ligands for CD1a, and can be presented to CD1a-restricted T cells from human skin. We believe that this is an important finding, not only for CD1a and Langerhans cell biology, but for many forms of cutaneous inflammation and is a key focus of our ongoing work. I continue to do two clinics per week in dermatology at the Churchill hospital. This has been invaluable as a resource for understanding disease and for access to clinical samples from well-defined cohorts and the translation of our findings to clinical trials.

What are the Future Aims of Your Current Group

The overall aim of the group is to understand the pathogenesis of cutaneous inflammatory disease in order to identify new approaches to disease prevention and treatment. The studies will contribute to our understanding of the interaction between the epithelium and the innate and adaptive immune response. Emphasis will be focused on: 1) understanding mechanisms underlying CD1a presentation of lipid antigens to T cells in the skin; 2) characterising the function of ILC2 in the skin, and the therapeutic implications; 3) how filaggrin insufficiency promotes atopic inflammation and whether this can be therapeutically modified; 4) investigating mechanisms underlying the cellular immune response to viral antigens in human skin. As well as contributing to disease and tissue specific questions, these studies will advance the broader Unit aims of defining the interactions between the innate and adaptive immune responses and the local micro-environment, which in turn will support the development of new approaches to vaccination and treatment.

How do the aims of your research fit with the aims of the WIMM and Division of Medicine?

The work of the group is directly informed by clinical observation from patients we see in clinic, and is then translated back to the patients. This is illustrated, for example, by the ILC2 work above, which is being explored through a clinical trial. We aim to understand disease by studying samples from humans, but also using models, as required, to investigate underlying mechanisms that may lead to opportunities for therapeutic intervention. In particular, I believe that the CD1a work is likely to be significance in many human skin diseases. As well as scientific research to contribute to the understanding and management of human disease, we are also contributing to the training of scientists and academic clinicians. Over the last 10 years, there have been 10 DPhils completed, of which 6 were by clinicians – there are five current DPhil students in the laboratory. There have been many others in training who have had periods in the laboratory including MSc students, medical students, academic F1/F2, clinical lecturers, academic clinical fellows and overseas visitors. We aim to function within networks to enhance opportunities for success, including integral links with the NIHR BRC, NHS, NIHR Comprehensive Research Network and we participate in local and multicenter clinical trials. The work involves local, national and international collaborations - key collaborators are Vincenzo Cerundolo, Paul Klenerman, Andrew McKenzie (LMB), Branch Moody (Harvard). We also contribute to the work of the institute towards the public understanding of science, including participation in National Science and Engineering Week (several talks) and the Royal Society Summer Exhibition (2002).

Lay Summary of Research

We are working towards treatment and prevention of skin disease. The skin is often the first point of contact with microbes and allergens, but relatively little is understood about how the cutaneous immune system clears these challenges. Such knowledge is vitally important to understanding the mechanisms of skin disease and related diseases, and for developing more effective ways of cutaneous drug and vaccine delivery.

It is increasingly clear that skin barrier dysfunction is an important first step in the development of atopic eczema, one of the commonest skin diseases in the UK, and often associated with asthma and rhinitis. The barrier dysfunction promotes entry of allergens and microbes which eventually lead to skin inflammation. The latter is treated with topical immune suppressants, but these are not curative and also carry risks of side effects.

We wish to understand the steps linking barrier dysfunction and skin inflammation, as these will provide opportunities for new treatments. In particular, we will explore ways to repair barrier function and to understand the roles of novel immune cells in contributing to the inflammation.

These findings will have implications for atopic eczema, but also for other forms of inflammatory skin disease and indeed for the improvement of vaccine delivery in to the skin.

All Publications Over the Past 5 Years

1. Xue L, Salimi M, Panse I, Mjosberg JM, McKenzie AN, Spits H, Klenerman P, Ogg G. Prostaglandin D2 activates group 2 innate lymphoid cells via CRTH2. Journal Allergy Clinical Immunology. 2014;133( 4):1184-94.

2. Xue L, Fergusson J, Salimi M, Panse I, Ussher J, Hegazy A, Hunter MG, Pettipher R, Ogg G, Klenerman P. Prostaglandin D2 and Leukotriene E4 synergise to stimulate diverse Th2 functions and Th2 cell/neutrophil crosstalk. Journal Allergy Clinical Immunology. 2014;in press.

3. Pan X, Huang LC, Dong T, Peng Y, Cerundolo V, McGowan S, Ogg G. Combinatorial HLA-peptide bead libraries for high throughput identification of CD8(+) T cell specificity. J Immunol Methods. 2014 Jan 31;403(1-2):72-8.

4. Oliphant CJ, Hwang YY, Walker JA, Salimi M, Wong SH, Brewer JM, Englezakis A, Barlow JL, Hams E, Scanlon ST, Ogg GS, Fallon PG, McKenzie AN. MHCII-Mediated Dialog between Group 2 Innate Lymphoid Cells and CD4 T Cells Potentiates Type 2 Immunity and Promotes Parasitic Helminth Expulsion. Immunity. 2014 Jul 30;41:283-95.

5. Marwah I, Wang X, Chan H, Ogg GS, Gutowska-Owsiak D. Filaggrin-insufficiency in keratinocytes influences responsiveness of allergen-specific T cells to cognate antigen and compounds barrier function deficiency. Clin Immunol. 2014 Jul;153(1):153-5.

6. Gutowska-Owsiak D, Selvakumar TA, Salimi M, Taylor S, Ogg GS. Histamine enhances keratinocyte-mediated resolution of inflammation by promoting wound healing and response to infection. Clin Exp Dermatol. 2014 Mar;39(2):187-95.

7. Gutowska-Owsiak D, Greenwald L, Watson C, Selvakumar TA, Wang X, Ogg GS. Histamine synthesizing enzyme, histidine decarboxylase, is upregulated by keratinocytes in atopic skin. Br J Dermatol. 2014 Jun 24.

8. Wang X, Salimi M, Gutowska-Owsiak D, Ogg G. Filaggrin modulates the proliferation, differentiation and apoptosis of keratinocytes. Submitted. 2013.

9. Vukmanovic-Stejic M, Sandhu D, Sobande TO, Agius E, Lacy KE, Riddell N, Montez S, Dintwe OB, Scriba TJ, Breuer J, Nikolich-Zugich J, Ogg G, Rustin MH, Akbar AN. Varicella zoster-specific CD4+Foxp3+ T cells accumulate after cutaneous antigen challenge in humans. J Immunol. 2013 Feb 1;190(3):977-86.

10. Salimi M, Barlow JL, Saunders SP, Xue L, Gutowska-Owsiak D, Wang X, Huang L, Johnson D, Scanlon ST, McKenzie AN, Fallon GP, Ogg G. A role for IL-25 and IL-33-driven type-2 innate lymphoid cells in atopic dermatitis. Journal of Experimental Medicine. 2013;210:2939-50.

11. Malavige GN, Jeewandara C, Alles KM, Salimi M, Gomes L, Kamaladasa A, Jayaratne SD, Ogg GS. Suppression of virus specific immune responses by IL-10 in acute dengue infection. PLoS Negl Trop Dis. 2013;7(9):e2409.

12. Malavige GN, Gomes L, Alles L, Chang T, Salimi M, Fernando S, Nanayakkara KD, Jayaratne S, Ogg GS. Serum IL-10 as a marker of severe dengue infection. BMC Infect Dis. 2013;13(1):341.

13. Malavige G, Ogg G. T cell responses in dengue viral infections. Journal Clinical Virology. 2013;58:605-11.

14. Lohitharajah J, Malavige GN, Wijewickrama A, Ambagawita A, Seneviratne AL, Ogg G. Molecular characterisation of varicella zoster virus genotypes in Sri Lanka. Ceylon Med J. 2013 Dec;58(4):153-6.

15. Huang L, Pan X, Yang H, Wan LKD, Stewart-Jones G, Dorrell L, Ogg G. Linking genotype to phenotype on beads: high throughput selection of peptides with biological function. Scientific Reports. 2013;3:3030.

16. Gutowska-Owsiak D, Salimi M, Selvakumar TA, Wang X, Taylor S, Ogg G. Histamine exerts multiple effects on expression of genes associated with epidermal barrier function. J Investig Allergol Clin Immunol. 2013;24:231-9.

17. Gutowska-Owsiak D, Ogg GS. Cytokine regulation of the epidermal barrier. Clin Exp Allergy. 2013 Jun;43(6):586-98.

18. Xue L, Barrow A, Fleming VM, Hunter MG, Ogg G, Klenerman P, Pettipher R. Leukotriene E4 activates human Th2 cells for exaggerated proinflammatory cytokine production in response to prostaglandin D2. J Immunol. 2012 Jan 15;188(2):694-702.

19. Malavige GN, McGowan S, Atukorale V, Salimi M, Peelawatta M, Fernando N, Jayaratne SD, Ogg G. Identification of serotype-specific T cell responses to highly conserved regions of the dengue viruses. Clin Exp Immunol. 2012 May;168(2):215-23.

20. Malavige G, Ogg G. Pathogenesis of severe dengue infection. Ceylon Medical Journal. 2012;57:97-100.

21. Malavige G, Huang L, Salimi M, Gomes L, Jayaratne SD, Ogg G. Cellular and cytokine correlates of severe dengue infection. PLoS ONE. 2012;7(11):e50387.

22. Jayaratne SD, Gomes L, Ogg G, Malavige G. Evaluation of the WHO revised criteria for classification of clinical disease severity in acute adult dengue infection. BMC Research. 2012;In press.

23. Gutowska-Owsiak D, Schaupp AL, Salimi M, Selvakumar TA, McPherson T, Taylor S, Ogg GS. IL-17 downregulates filaggrin and affects keratinocyte expression of genes associated with cellular adhesion. Exp Dermatol. 2012 Feb;21(2):104-10.

24. Gutowska-Owsiak D, Ogg GS. The epidermis as an adjuvant. J Invest Dermatol. 2012 Mar;132(3 Pt 2):940-8.

25. Gutowska-Owsiak D, Ogg G. Cytokine regulation of the epidermal barrier. Clinical & Experimental Allergy. 2012;21(2):104-10.

26. Crack LR, Chan HW, McPherson T, Ogg GS. Identification of an immunodominant region of the major house dust mite allergen Der p 2 presented by common human leucocyte antigen alleles. Clin Exp Dermatol. 2012 Apr;37(3):266-76.

27. Crack L, Jones L, Chan H, McPherson T, Ogg G. Human Anti-microbial Peptides LL-37 and Human β-defensin-2 reduce viral load replication in varicella zoster virus-vaccine infected keratinocytes. Clin Exp Dermatol. 2012;37:534-43.

28. Malavige GN, Rostron T, Rohanachandra LT, Jayaratne SD, Fernando N, De Silva AD, Liyanage M, Ogg G. HLA class I and class II associations in dengue viral infections in a Sri Lankan population. PLoS ONE. 2011;6(6):e20581.

29. Gutowska-Owsiak D, Schaupp AL, Salimi M, Taylor S, Ogg GS. Interleukin-22 downregulates filaggrin expression and affects expression of profilaggrin processing enzymes. Br J Dermatol. 2011 Sep;165(3):492-8.

30. Gomes PL, Malavige GN, Fernando N, Mahendra MH, Kamaladasa SD, Seneviratne JK, Karunatilaka DH, Ogg GS. Characteristics of Staphylococcus aureus colonization in patients with atopic dermatitis in Sri Lanka. Clin Exp Dermatol. 2011 Mar;36(2):195-200.

31. Crack LR, Chan HW, McPherson T, Ogg GS. Phenotypic analysis of perennial airborne allergen-specific CD4+ T cells in atopic and non-atopic individuals. Clin Exp Allergy. 2011 Nov;41(11):1555-67.

32. Aslam A, Lloyd-Lavery A, Warrell DA, Misbah S, Ogg GS. Common filaggrin null alleles are not associated with hymenoptera venom allergy in Europeans. Int Arch Allergy Immunol. 2011;154(4):353-5.

33. Aslam A, Chapel H, Ogg G. Direct ex-vivo evaluation of pneumococcal specific T-cells in healthy adults. PLoS ONE. 2011;6(10):e25367.

34. Aly L, Yousef S, Schippling S, Jelcic I, Breiden P, Matschke J, Schulz R, Bofill-Mas S, Jones L, Demina V, Linnebank M, Ogg G, Girones R, Weber T, Sospedra M, Martin R. Central role of JC virus-specific CD4+ lymphocytes in progressive multi-focal leucoencephalopathy-immune reconstitution inflammatory syndrome. Brain. 2011 Sep;134(Pt 9):2687-702.