Undergraduate medical training at the Charité Medical University Berlin, Germany. Research degree (Dr.med.) in pharmacology with thesis on nitric oxide receptor (summa cum laude, 1996). 1997 - 2000 post-doctoral scientist with Ivan Horak at the Institute for Molecular Pathology, Berlin (immune-pathogenesis in IRF8-deficient mice). 2000 – 2004 specialist training in Dermatology at the Charité Medical University with research focus on immune-pathogenesis in psoriasis. Certified specialist in Dermatology (2004), sub-certified in Allergy (2005). 2004 – 2007 consultant dermatologist at Charité Medical University Berlin; clinics in general dermatology and immune-dermatology; career-development grant by Deutsche Forschungsgemeinschaft. Continued research in genetics and immune-pathogenesis of psoriasis, clinical research in scleroderma (see Publications). 2007 – 2009 fellow in cancer immunology, University of Dundee and honoroary loc. Consultant (NHS). 2009 – present senior clinical lecturer, continued work in immune-pathogenesis of psoriasis, and immune-pathology of skin cancer (see Publications). 2010 – present, GCP-certified; local site coordinator of psoriasis clinical research; principle investigator in early and late phase multi-center trials of immune-intervention in psoriasis.

West J, Ogston S, Foerster J, Safety and efficacy of methotrexate in psoriasis: a meta-analysis of published trials, PLoS ONE, 2016, in press West J, Ogston S, Palmer C, Fleming C, Dawe R, Kumar V, Waterston S, Foerster J., Methotrexate in psoriasis under real world conditions: long-term efficacy and tolerability, Br J Dermatol. 2016 Feb 6 Foerster J, Bachman M. Beyond passive immunization: toward a nanoparticle-based IL-17 vaccine as first in class of future immune treatments, Nanomedicine (Lond). 2015;10(8):1361-9. doi: 10.2217/nnm.14.215. Ali FR, Barton A, Smith RL, Bowes J, Flynn E, Mangino M, Bataille V, Foerster JP, Worthington J, Griffiths CE, Warren RB (2013), An investigation of rheumatoid arthritis loci in patients with early-onset psoriasis validates association of the REL gene, Br J Dermatol. 2013 Apr;168(4):864-6 Hack K, Reilly L, Palmer C, Read KD, Norval S, Kime R, Booth K, Foerster J, Skin-targeted inhibition of PPAR β/δ by selective antagonists to treat PPAR β/δ-mediated psoriasis-like skin disease in vivo, PLoS One. 2012;7(5):e37097. Lai OY, Chen H, Michaud HA, Hayashi G, Kuebler PJ, Hultman GK, Ariza ME, Williams MV, Batista MD, Nixon DF, Foerster J, Bowcock AM, Liao W, Protective effect of human endogenous retrovirus K dUTPase variants on psoriasis susceptibility, J Invest Dermatol. 2012 Jul;132(7):1833-40 Pourreyron C, Reilly L, Proby C, Panteleyev A, Fleming A, McLean K, South AP, Foerster J (2012), Wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical Wnt signalling is repressed, PloS ONE, 7(2):e3182 Hack K, Reilly L, Proby C, Fleming C, Leigh I, Foerster J (2012) Wnt5a inhibits the CpG-ODN triggered activation of human plasmacytoid dendritic cells, Clin Exp Dermatol, 37(5):557-61 Watt SA, Pourreyron C, Purdie K, [..],Foerster J, Leigh IM, South AP (2011) Integrative mRNA profiling comparing cultured primary cells with clinical samples reveals PLK1 and C20orf20 as therapeutic targets in cutaneous squamous cell carcinoma. Oncogene. 30(46):4666-77 Romanowska M, Reilly L, Palmer C, Gustaffson M, Foerster J (2010) “Activation of PPAR beta/delta causes a psoriasis like skin disease in vivo”, PLoS ONE, 5(3): e9701 Romanowska M, Evans A, Kellock D, Bray SE, McLean K, Donandt S, Foerster J. (2009) “Wnt5a exhibits layer-specific expression in adult skin, is upregulated in psoriasis, and synergizes with type 1 interferon.” PLoS ONE. 2009;4(4):e5354. Epub 2009 Apr 28. Krauss S, Foerster J, Schneider R, Schweiger S. (2008). “Protein phosphatase 2A and rapamycin regulate the nuclear localization and activity of the transcription factor GLI3.” Cancer Res. 2008 Jun 15;68(12):4658-65. Al Yacoub, N., Romanowska, M., Foerster, J. (2008). “PPAR delta is a target gene of type 1 interferon and inhibits apoptosis in human T cells”, J Invest Dermatol., 128 (8), 1940 - 9 Romanowska M, Al Yacoub N, Seidel H, Donandt S, Gerken H, Phillip S, Sterry W, Foerster J (2008) PPARdelta Enhances Keratinocyte Proliferation in Psoriasis and Induces Heparin-Binding EGF-Like Growth Factor. J Invest Dermatol., 128 (1), 110-24 al Yacoub N, Romanowska M, Haritonova N, Foerster J (2007) Optimized production and concentration of lentiviral vectors containing large inserts. The Journal of Gene Medicine 9:579-584. Foerster J, Nolte I, Junge J, Bruinenberg M, Schweiger S, Spaar K, et al. (2005) Haplotype sharing analysis identifies a retroviral dUTPase as candidate susceptibility gene for psoriasis. J Invest Dermatol 124:99-102. Foerster J, Nolte I, Schweiger S, Ehlert C, Bruinenberg M, Spaar K, et al. (2004) Evaluation of the IRF-2 gene as a candidate for PSORS3. J Invest Dermatol 122:61-64. Trockenbacher A, Suckow V, Foerster J, Winter J, Krauss S, Ropers HH, et al. (2001) MID1, mutated in Opitz syndrome, encodes an ubiquitin ligase that targets phosphatase 2A for degradation. Nat Genet 29:287-294. Schweiger S, Foerster J, Lehmann T, Suckow V, Muller YA, Walter G, et al. (1999) The Opitz syndrome gene product, MID1, associates with microtubules. Proc Natl Acad Sci U S A 96:2794-2799. Scheller M, Foerster J, Heyworth CM, Waring JF, Lohler J, Gilmore GL, et al. (1999) Altered development and cytokine responses of myeloid progenitors in the absence of transcription factor, interferon consensus sequence binding protein. Blood 94:3764-3771. Rosenbauer F, Waring JF, Foerster J, Wietstruk M, Philipp D, Horak I (1999) Interferon consensus sequence binding protein and interferon regulatory factor-4/Pip form a complex that represses the expression of the interferon-stimulated gene-15 in macrophages. Blood 94:4274-4281. Friebe A, Wedel B, Harteneck C, Foerster J, Schultz G, Koesling D (1997) Functions of conserved cysteines of soluble guanylyl cyclase. Biochemistry 36:1194-1198. Foerster J, Harteneck C, Malkewitz J, Schultz G, Koesling D (1996) A functional heme-binding site of soluble guanylyl cyclase requires intact N-termini of alpha 1 and beta 1 subunits. Eur J Biochem240:380-386. Wedel B, Humbert P, Harteneck C, Foerster J, Malkewitz J, Bohme E, et al. (1994) Mutation of His-105 in the beta 1 subunit yields a nitric oxide-insensitive form of soluble guanylyl cyclase. Proc Natl Acad Sci U S A 91:2592-2596