Dr Graham Wallace BSc, PhD

Institute of Inflammation and Ageing
Senior Lecturer in Immunity and Infection

Contact details

Address
Centre for Translational Inflammation Research
University of Birmingham Research Laboratories
Queen Elizabeth Hospital
University of Birmingham
Edgbaston
Birmingham, B15 2TT

Graham Wallace is a Senior Lecturer in the Institute of Inflammation and Ageing. 

Graham has published over 75 research papers in scientific journals as well as reviews in the fields of ocular immunology, Behcet’s Disease and immunogenetics. He has received grants from Guide Dogs for the Blind Association, Fight for Sight, and the Wellcome Trust. 

He is an enthusiastic communicator on the theme immune responses in the eye and the effects of gene polymorphgisms on ocular diseases. Graham is on the Medical Panel of the Behcet’s Syndrome Society and speaks at meetings of patient groups on a regular basis

Qualifications

  • PhD Immunology 1988
  • BSc Immunology 1985

Biography

Graham Wallace qualified with a BSc Immunology from the University of London in 1985. He went on to study for a PhD in Immunology at University College London which was awarded in 1988. Following a postdoctoral position at the London School of Hygiene and Tropical Medicine , London Graham started a postdoctoral position at St Thomas’ Hospital London in ocular immunology. One of the diseases that was of interest to the group was Behcet’s Disease. That initiated his interest in the condition, and it has been part of his laboratory’s work ever since. Behcet’s is an immunological enigma and therefore provides many interesting avenues for research. A particular interest is the genetic basis of the disease as the geographical spread suggests an aetiology that matches the name the Silk Road disease. This work on the immunogenetic basis of ocular disease is at the forefront of current studies and is being prepared as a major review which we believe will alter the current paradigms. Samples from his DNA bank collected from patients at Birmingham, London and the Middle East are currently being used in further studies by colleagues in Leeds, Dublin, Rotterdam and Lisbon, and Portland, Oregon.

In the broader field of inflammatory eye disease (uveitis) the effects of the local environment on inmmune response is a major part of Graham’s work. In a particular, the role of endogenous cortisol and vitamin D3 production on responses in ocular cells is investigated. The use of pathological specimens to study these elements has been a significant theme in Graham research.

Teaching

Teaching Programmes

Postgraduate supervision

Graham is interested in supervising doctoral research students in the following areas:

  • The effect of vitamin D production in ocular barrier cells
  • Biological dressings for treating corneal infectious disease
  • The genetic basis of ocular inflammatory disease

If you are interesting in studying any of these subject areas please contact Graham on the contact deatils above, or for any general doctoral research enquiries, please email: dr@contacts.bham.ac.uk or call +44 (0)121 414 5005.

For a full list of available Doctoral Research opportunities, please visit our Doctoral Research programme listings

Research

RESEARCH THEMES

Ocular Immunology, Behcet’s Disease, Immunogenetics 

RESEARCH ACTIVITY

Behcet’s Disease (BD)

In Behcet’s Disease, in collaboration with colleagues in Birmingham (PI Murray), London (Prof MR Stanford, King’s College and Prof Farida Fortune, Queen Mary’s College) and Professor Rob Moots (University of Liverpool, Graham has identified several single nucleotide polymorphisms (SNP) including those associated with increased production of tumour necrosis factor, and Factor V Leiden, both linked to severe vascular disease (retinal occlusion), and MHC class I-related protein MICA*009, which I have postulated is involved in control and licensing of NK cells (see below). Recently, Graham has analysed SNP in PTPN22 and CTLA-4, two genes regarded as genetic masterswitches for autoimmunity, and found that CTLA-4 SNP were not associated with BD, while PTPN22 620W was inversely associated. These results support the view that BD is an autoinflammatory condition and not autoimmune. Recent work has focussed on the evolutionary aspect of gene mutations in BD.

Ocular Immunology

Research has focussed on the effect of the ocular microenvironment on macrophage activation by Toll-like receptor ligands, to address the conditions in which immune privilege may be maintained or broken. In related studies, in collaboration with Miss Si Rauz (Institute of Inflammation and Ageing) the effect of TLR signalling on antimicrobial defensins and chemokine production by corneal epithelial cells is being addressed. The effects of TLR stimulation are being analysed in the presence of both cortisol and vitamin D3 production to investigate interaction between these endogenous (protective) and exogenous (inflammatory pathways. The results have shown for the first time that corneal epithelial cells can make active vitamin D3, while fibroblasts make active cortisol, but that neither affects TLR stimulation.

On the cellular side with in collaboration with Professor Farida Fortune, Professor Miles Stanford and Dr Harry Petrushkin, Graham has investigated the functional relevance of the HLA-MICA coexpression identified by his genetic studies in BD. The results show that while a differential response of inhibition of killing in patients compared to controls. This may have an important effect on NK cell function and we are currently sequencing the molecules involved in NK control.

Other activities

  • Honorary Secretary of The International Society for Behcet’s Disease
  • Vice-President and President-elect of the International Society of Inflammation Societies
  • Deputy Director of the Graduate School of the College of Medical and Dental Sciences

Publications

Anuforom O, Wallace GR, Buckner MM and Piddock LJ (2016) Ciprofloxacin and ceftriaxone alter cytokine responses, but not Toll-like receptors, to Salmonella infection in vitro. J Antimicrob Chemother 71(7):1826-33

Morton LT, Situnayake D and Wallace GR (2016) Genetics and epigenetics of Behçet's syndrome. Curr Opin Rheumatol 28(1):39-44

Petrushkin H, Thomas D, Vaughan R, Kondeatis E, Stanford MR,  Edelsten C and Wallace GR (2015) Possession of the HLA-DRB1*1501 allele and visual outcome in idiopathic intermediate uveitis. JAMA Ophthalmol 133(4):482-3

Petrushkin H, Hasan MS, Stanford MR, Fortune F and Wallace GR (2015) Behcet’s Disease: Do natural killer cells play a significant role? Front Immunol 6:134

Kappen JH, Medina-Gomez C, van Hagen PM, Stolk L, Estrada K, Rivadeneira F, Uitterlinden AG, Stanford MR, Ben-Chetrit E, Wallace GR, Soylu M and van Laar JA (2015) Genome-wide association study in an admixed case series reveals IL12A as a new candidate in Behçet disease. PLoS One 10(3):e0119085

Riddell NE, Burns VE, Wallace GR, Edwards KM, Drayson M, Redwine LS, Hong S, Bui JC, Fischer JC, Mills PJ and Bosch JA (2015) Progenitor cells are mobilized by acute psychological stress but not beta-adrenergic receptor agonist infusion. Brain Behav Immun 49:49-53

Barry RJ, Alsalem JA, Faassen J, Murray PI, Curnow SJ and Wallace GR (2015) Association analysis of TGFBR3 gene with Behçet’s Disease and Idiopathic Intermediate Uveitis in a Caucasian population. Br J Ophthalmol 99(5):696-9

Zalli A, Bosch JA, Goodyear O, Riddell N, McGettrick HM, Moss P and Wallace GR (2015) Targeting β2 adrenergic receptors regulate human T cell function directly and indirectly Brain Behavior and Immunity. Brain Behav Immun 45:211-8

Alsalem JA, Patel D, Susarla R, Coca-Prados M, Bland R, Walker EA, Rauz S and Wallace GR (2014) Characterization of Vitamin D Production by Human Ocular Barrier Cells. Invest Ophthalmol Vis Sci 55(4):2140-7

Susarla R,  Liu L, Walker EA, Bujalska IJ, Alsalem JA, Williams GP, Sreekantam S, Taylor AE, Tallouzi M, Southworth HS, Murray PI, Wallace GR and Rauz S (2014) Cortisol Biosynthesis in the Human Ocular Surface Innate Immune Response. PLoS One 9(4):e94913

Wallace GR (2014) HLA-B*51 the primary risk in Behçet disease. Proc Natl Acad Sci U S A 111(24):8706-7

Lee YJ, Horie Y, Wallace GR, Choi YS, Park JA, Song R, Kang YM, Kang SW, Baek HJ, Kitaichi N, Meguro A, Mizuki N, Namba K, Ishida S, Kim J, Niemczek E, Lee EY, Song YW, Ohno S and Lee EB (2013) Genome-wide association study identifies GIMAP as a novel susceptibility locus for Behçet’s disease. Ann Rheum Dis 72(9):1510-6

Quax RA, van Laar JAM, van Heerebeek R, Greiner K, Ben-Chetrit E, Stanford M, Wallace GR, Fortune F, Ghabra M, Soylu M, Hazes JM, Lamberts SW, Kappen JH, van Hagen PM, Koper JW and Feelders RA (2012) Glucocorticoid sensitivity in Behçet's disease. Endocr Connect 1(2):103-11

Shafi S, Vantourout P, Wallace G, Antoun A, Vaughan R, Stanford M and Hayday A (2011) An NKG2D-mediated human lymphoid stress surveillance response with high interindividual variationSci Transl Med 3(113):113ra124

Remmers EF, Cosan F, Kirino Y, Ombrello MJ, Abaci N, Satorius C, Le JM,  Yang B, Korman BD, Cakiris A, Aglar O, Emrence Z, Azakli H, Ustek D, Tugal-Tutkun I, Akman-Demir G, Chen W, Amos CI, Dizon MB, Kose AA, Azizlerli G, Erer B, Brand OJ, Kaklamani VG, Kaklamanis P, Ben-Chetrit E, Stanford M, Fortune F, Ghabra M, Ollier WE, Cho YH, Bang D, O'Shea J, Wallace GR, Gadina M, Kastner DL and Gül A (2010) Genome-wide association study identifies variants in MHC class I, IL10 and IL23R-IL12RB2 regions associated with Behcet’s Disease. Nat Genet 42(8):698-702