Dr Anna Ridley, BSc, MSc, DPhil

Profile

After completing my undergraduate studies in Biology at the University of Southampton I trained as a Clinical Scientist in Immunology at Southampton General Hospital, during which time I undertook an MSc in Medical Immunology at King’s College London. Following this I spent a year monitoring clinical trials at Oxford BioMedica and subsequently moved to the University of Oxford as a research assistant, then completed a DPhil investigating T cell phenotype and function in inflammatory arthritis. As a postdoc, also in Oxford, my research focused on using cellular techniques to investigate T cells and neutrophils in inflammatory arthritis and I became involved in teaching, including lecturing, running departmental workshops and supervising students in the lab. My interest in teaching led me to pursue a PGCert in Teaching and Learning in Higher Education, gaining Fellowship of the HEA, and precipitated my move into a purely teaching role at Queen Mary University of London, as a Lecturer in Immunology and Infection. I am passionate about communicating science and as a STEM ambassador work with teachers to engaged students.

Teaching

• Core teaching team for MSc Biomedical Science (Medical Microbiology), MSc Clinical Science (infection Science) and MSc Clinical Microbiology
• Lecturer in Immunology in the Nanchang University Joint Programme (Basic Immunology)
• Problem Based Learning (tutor) for undergraduate medical students – MBBS 

Research

Research Interests:

I am interested in defining the phenotype and function of T cells from patients with inflammatory arthritis. Using cellular techniques, I have screened compounds identified by artificial intelligence with the aim of finding new treatments for this disease. A further interest is the innate immune system in inflammatory arthritis and specifically how neutrophils, an abundant but understudied population, are involved in disease pathogenesis.

Publications

• Simone D, Penkava F, Ridley A, Sansom S, Al-Mossawi MH, Bowness P. (2021). "Single cell analysis of spondylarthritis regulatory T cells identifies distinct synovial gene expression patterns and clonal fate." Commun Biol. 4(1):1395
• Al-Mossawi MH, Chen L, Fang H, Ridley A, de Wit J, Yager N, Hammitzsch A, Pulyakhina I, Fairfax BP, Simone D, Yi Y, Bandyopadhyay S, Doig K, Gundle R, Kendrick B, Powrie F, Knight JC, Bowness P. (2017).  "Unique transcriptome signatures and GM-CSF expression in lymphocytes from patients with spondyloarthritis." Nat Commun. 8(1):1510.
• Ridley A., Hatano H., Wong-Baeza I., Shaw J., Matthews KK., Al-Mossawi H., Ladell K., Price DA., Bowness P. and Kollnberger S. (2016). "Activation-induced KIR3DL2 binding to HLA-B27 licenses pathogenic T cell differentiation in Spondyloarthritis." Arthritis Rheumatol. 68(4): 901-14
• Wong-Baeza, I., Ridley, A., Shaw, J., Hatano, H., Rysnik, O., McHugh, K., Piper, C., Brackenbridge, S., Fernandes, R., Chan, A., Bowness, P., and Kollnberger, S. (2013). "KIR3DL2 Binds to HLA-B27 Dimers and Free H Chains More Strongly than Other HLA Class I and Promotes the Expansion of T Cells in Ankylosing Spondylitis." J Immunol. 190(7): 3216-24
• Bowness, P., Ridley, A., Shaw, J., Chan, A. T., Wong-Baeza, I., Fleming, M., Cummings, F., McMichael A. and Kollnberger, S. (2011). "Th17 cells expressing KIR3DL2+ and responsive to HLA-B27 homodimers are increased in ankylosing spondylitis." J Immunol 186(4): 2672-80.