Hayley Eames

I joined the Kennedy Institute of Rheumatology in 2009 with a keen interest in macrophage biology, following my BSc (University of Bath) where I studied macrophage-like hemocytes in Drosophila development, and an industrial placement year at GlaxoSmithKline studying macrophage polarisation. My PhD in molecular immunology focussed on regulation of inflammatory gene expression by the transcription factor Interferon Regulatory Factor 5 (IRF5), which is primarily expressed in inflammatory myeloid cells.  Mice deficient in IRF5 have been shown to be resistant to septic shock and to produce a reduced amount of pro-inflammatory cytokines, leading to T_H2 rather than T_H1 responses. Proteomic screens were performed to identify novel transcriptional co-factors of IRF5. In particular, TRIM28/KAP1 was identified as a novel epigenetic inhibitor of IRF5-mediated TNFɑ expression in macrophages. The interaction of IRF5 with the RelA subunit of NFκB was also characterised, parallel to genome-wide ChIPseq studies that implicated IRF5 and RelA in co-operative regulation of a large subset of inflammatory genes in macrophages.

As a post-doctoral scientist my interests still lie with innate immunity, but have now expanded to include neutrophils; following our discovery in the Udalova laboratory that IFNλ2 (IL28A) treatment in the CIA model of arthritis completely abrogates disease and reverses joint damage, via inhibition of IL-1β-mediated neutrophil recruitment to the joint. My research now focusses on the molecular mechanisms of this inhibition, and in translation of these findings to human autoimmune diseases such as Rheumatoid Arthritis and Vasculitis.