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Dr. Conor Finlay
Research Fellow, Clinical Medicine

Publications and Further Research Outputs

Peer-Reviewed Publications

Cunningham Kyle , Finlay Conor , Mills Kingston H, Helminth Imprinting of Hematopoietic Stem Cells Sustains Anti-Inflammatory Trained Innate Immunity That Attenuates Autoimmune Disease, Journal of Immunology, 206, (7), 2021, p1618 - 1630 Journal Article, 2021 DOI URL

Finlay Conor , Allen Judith, The immune response of inbred laboratory mice to Litomosoides sigmodontis : A route to discovery in myeloid cell biology, 42, (7), 2020, pe12708 - e12708 Journal Article, 2020 URL DOI

Finlay, C.M. and Cunningham, K.T. and Doyle, B. and Mills, K.H.G., IL-33-stimulated murine mast cells polarize alternatively activated macrophages, which suppress T cells that mediate experimental autoimmune encephalomyelitis, Journal of Immunology, 205, (7), 2020, p1909-1919 Journal Article, 2020 DOI

McEntee, C.P. and Finlay, C.M. and Lavelle, E.C., Divergent roles for the IL-1 family in gastrointestinal homeostasis and inflammation, Frontiers in Immunology, 10, (JUN), 2019 Journal Article, 2019 TARA - Full Text DOI

Czajkowska Beata I, Finlay Conor , Jones Glyni, Brown Terence A, Diversity of a cytokinin dehydrogenase gene in wild and cultivated barley, 14, (12), 2019, pe0225899 - e0225899 Journal Article, 2019 URL DOI

Campbell Sharon , Knipper Johanna , Ruckerl Domini, Finlay Conor , Logan Nicol, Minutti Carlos , Mack Matthia, Jenkins Stephen , Taylor Matthew , Allen Judith, Myeloid cell recruitment versus local proliferation differentiates susceptibility from resistance to filarial infection, 7, 2018, pe30947 - e30947 Journal Article, 2018 URL DOI

Sutton, C.E. and Finlay, C.M. and Raverdeau, M. and Early, J.O. and DeCourcey, J. and Zaslona, Z. and O'Neill, L.A.J. and Mills, K.H.G. and Curtis, A.M., Loss of the molecular clock in myeloid cells exacerbates T cell-mediated CNS autoimmune disease, Nature Communications, 8, (1), 2017, p1923- Journal Article, 2017 DOI TARA - Full Text

Finlay, C.M. and Stefanska, A.M. and Coleman, M.M. and Jahns, H. and Cassidy, J.P. and McLoughlin, R.M. and Mills, K.H.G., Secreted products of Fasciola hepatica inhibit the induction of T cell responses that mediate allergy, Parasite Immunology, 39, (10), 2017, pe12460 - Journal Article, 2017 DOI

Finlay CM, Stefanska AM, Walsh KP, Kelly PJ, Boon L, Lavelle EC, Walsh PT, Mills KH., Helminth Products Protect against Autoimmunity via Innate Type 2 Cytokines IL-5 and IL-33, Which Promote Eosinophilia., Journal of Immunology, 196, (2), 2016, p703-714 Journal Article, 2016 DOI

Bernard NJ, Finlay CM, Tannahill GM, Cassidy JP, O'Neill LA, Mills KH, A critical role for the TLR signaling adapter Mal in alveolar macrophage-mediated protection against Bordetella pertussis., Mucosal immunology, 8, (5), 2015, p982 - 992 Journal Article, 2015 DOI

Finlay CM, Walsh KP, Mills KH, Induction of regulatory cells by helminth parasites: exploitation for the treatment of inflammatory diseases., Immunological reviews, 259, (1), 2014, p206-30 Journal Article, 2014 DOI

Coleman, M.M., Finlay, C.M., Moran, B., Keane, J., Dunne, P.J., Mills, K.H., The immunoregulatory role of CD4 +FoxP3 +CD25 - regulatory T cells in lungs of mice infected with Bordetella pertussis, FEMS Immunology and Medical Microbiology, 64, (3), 2012, p413-424 Journal Article, 2012 DOI TARA - Full Text

Walsh, KP, Brady, MT, Finlay, CM, Boon, L, Mills, KH, Infection with a helminth parasite attenuates autoimmunity through TGF-beta-mediated suppression of Th17 and Th1 responses., Journal of Immunology , 183, (3), 2009, p1577 - 1586 Journal Article, 2009 DOI TARA - Full Text

Research Expertise

Projects

  • Title
    • Macrophages in type 2 immunity: unravelling susceptibility and resistance to tissue nematode infection
  • Summary
    • Helminth infection is characterised by a type 2 immune response with polarisation of macrophages toward an M(IL-4) phenotype. It is increasingly recognised that macrophage functionality relies not only on direct cytokine signals but cellular origin and tissue environment. This programme is built around the pleural cavity, a tissue containing two predominant macrophage populations: monocyte-derived small cavity macrophages (SCMac) and large cavity macrophages (LCMac) which have a 'residency' gene expression module, conferred by the tissue niche. We will use the filarial nematode Litmosoides sigmodontis (Lito) as a model of pleural infection and as a tool to study M(IL-4) cells more generally. Mirroring divergent outcomes in human filariasis, susceptibility to Lito infection is dependent on host genotype, with striking differences in M(IL-4) cells between resistant and susceptible strains of mice. In resistant C57BL/6 mice LCMac expand greatly through proliferation and become M(IL-4) polarised. In susceptible BALB/c mice there are relatively more SCMac like cells which appear incapable of acquiring a full LCMac-residency or M(IL-4) programme. Aim 1 seeks to explain if strain differences are a result of intrinsic differences in macrophage programming, alterations of the tissue niche or due to differences in Th2 cell activity. The next 2 aims focus on resistant C57BL/6 mice as a model of type 2 immunity culminating in worm killing. Aim 2 looks upstream of macrophages to identify the cell-cell interactions in the pleural cavity and essential co-factors that drive M(IL-4) polarisation and proliferation. Aim 3 will look downstream of M(IL-4) cells to assess their contribution to worm killing and tissue integrity in the pleural cavity using mice which lack specific residency, M(IL-4) or proliferation gene modules. This programme will advance our knowledge of the activation and function of M(IL-4) cells and provide novel information on the function of the pleural space.
  • Funding Agency
    • Medical Research Council
  • Title
    • COVID-19 Strategic Partnership
  • Summary
    • Work package 2 'Immune responses and disease pathogenesis in COVID-19 patients
  • Funding Agency
    • SFI
  • Date From
    • 01/03/2021
  • Title
    • Nanoparticle modulation of neutrophil and monocyte responses to ANCA'
  • Summary
    • ANCA Vasculitis is a potentially lethal autoimmune disease, whereby the immune system is triggered to self-destruct - the systems normally primed to fight infection and cancer cells are incorrectly activated, resulting in damage to the blood vessels and eventually organ destruction, such as kidney failure. Auto-antibodies (proteins against oneself) bind to immune cells (neutrophils and monocytes) in the blood, improperly activating these cells and driving the development of ANCA vasculitis. The exact cause of ANCA vasculitis has yet to be discovered. Evidence suggests there is a complex interaction between a person's genetic make-up and unknown triggers in their environment. Silica dust, a common occupational hazard for construction workers amongst others, is the leading proposed environmental toxin. However, how exposure to silica influences the development of ANCA-vasculitis is unknown. We will address this by exploring the effects of silica on the same auto antibody-activated immune cells, which underpin ANCA vasculitis. These experiments will help explain the early events in ANCA vasculitis and may help to identify new treatments for this disease.
  • Funding Agency
    • TTMI - internal
  • Date From
    • 19/04/2021

Recognition

Memberships

British society of Immunology 29/09/2019 – 29/09/2022