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Dr. Conor Finlay

Senior Research Fellow (Trinity Translational Medicine Institute)
      
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Dr. Conor Finlay

Senior Research Fellow (Trinity Translational Medicine Institute)

 cofinlay@tcd.ie

 


I started my career at Trinity College Dublin under Prof Kingston Mills, where I used pre-clinical models of autoimmunity to identify pathways that shut down inflammation. I focused on how anti-inflammatory `type 2" immune responses regulated the inflammatory `type 1" responses. My interest in type 2 immune responses and myeloid cells brought me to a world-leading macrophage lab at the University of Manchester, under Prof Judi Allen. In Manchester, I retrained in bioinformatics, enabling me to understand project delivery from a multi-disciplinary point of view. Most recently, I moved into translational research at the Trinity Translational Medicine Institute (TTMI) gaining skills in patient-focused research, including in clinical data analysis and study design and facilitating collaboration with clinician-scientitst.
  Bioinformatics   Biomarkers of disease   Biomedical sciences   Biostatistical methods   Chronic inflamation   FLOW CYTOMETRY   GENE-EXPRESSION   Health informatics   Host, Pathogen interactions   Immune system   Immunology, Immunotherapy   INFECTION   Infectious diseases   INFLAMMATION   Inflammation and coagulation syndromes   Innate immunology   MACROPHAGES
Project Title
 Macrophages in type 2 immunity: unravelling susceptibility and resistance to tissue nematode infection
From
To
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
Programme
Programme Grant
Project Title
 Nanoparticle modulation of neutrophil and monocyte responses to ANCA'
From
19/04/2021
To
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
Programme
Building Engagements in Health Research
Project Title
 COVID-19 Strategic Partnership
From
01/03/2021
To
Summary
Work package 2 'Immune responses and disease pathogenesis in COVID-19 patients
Funding Agency
SFI
Project Title
 Understanding mast cells and their progenitors in Telangiectasia Macularis Eruptiva Perstans (TMEP)'
From
To
Summary
Funding Agency
TTMI - Internal
Programme
Building Engagements in Health Research Scheme
Project Title
 Mapping human macrophage anti-microbial function in pleural infection.
From
To
Summary
Funding Agency
Trinity College Dublin
Programme
Dean"s Research Initiatives Fund

Language Skill Reading Skill Writing Skill Speaking
English Fluent Fluent Fluent
Details Date From Date To
British society of Immunology 29/09/2019 29/09/2022
Han Jichan, Gallerand Alexandr, Erlich Emma C, Helmink Beth A, Mair Iri, Li Xi, Eckhouse Shaina R, Dimou Francesca M, Shakhsheer Baddr A, Phelps Hannah M, Chan Mandy M, Mintz Rachel L, Lee Daniel D, Schilling Joel D, Finlay Conor M, Allen Judith E, Jakubzick Claudia V, Else Kathryn J, Onufer Emily J, Zhang Na, Randolph Gwendalyn J, Human serous cavity macrophages and dendritic cells possess counterparts in the mouse with a distinct distribution between species, Nature Immunology, 25, (1), 2024, p155 - 165, Journal Article, PUBLISHED  DOI  URL
Ridge, Katie and Moran, Barry and Alvarado-Vazquez, P. Abigail and Hallgren, Jenny and Little, Mark A. and Irvine, Alan D. and O'Farrelly, Cliona and Dunne, Jean and co-senior). Finlay, Conor M (co-corresponding & and Conlon, Niall, Lin-CD117+CD34+FceRI+ progenitor cells are increased in chronic spontaneous urticaria and predict clinical responsiveness to anti-IgE therapy, Allergy, In Press, 2024, Journal Article, PUBLISHED
Finlay, Conor M and Allen, Judith E, IL-4-ever young: Type 2 cytokine signaling in macrophages slows aging., Immunity, 57, (3), 2024, p403--406 , Journal Article, PUBLISHED  DOI
Katie Ridge, Barry Moran, P. Abigail Alvarado"Vazquez, Jenny Hallgren, Mark A. Little, Alan D. Irvine, Cliona O'Farrelly, Jean Dunne, Conor M. Finlay, Niall Conlon, Lin"CD117+CD34+Fc"RI+ progenitor cells are increased in chronic spontaneous urticaria and predict clinical responsiveness to anti"IgE therapy, Allergy, 79, (9), 2024, p2423-2434 , Journal Article, PUBLISHED
Dwivedi, A. and Mhaonaigh, A.U. and Carroll, M. and Khosravi, B. and Batten, I. and Ballantine, R.S. and Phelan, S.H. and O†Doherty, L. and George, A.M. and Sui, J. and Hawerkamp, H.C. and Fallon, P.G. and Noppe, E. and Mason, S. and Conlon, N. and Cheallaigh, C.N. and Finlay, C.M. and Little, M.A., Emergence of dysfunctional neutrophils with a defect in arginase-1 release in severe COVID-19, JCI Insight, 9, (17), 2024, Notes: [cited By 0], Journal Article, PUBLISHED  TARA - Full Text  DOI
Conor M. Finlay, James E. Parkinson, Lili Zhang, Brian H.K. Chan, Jesuthas Ajendra, Alistair Chenery, Anya Morrison, Irem Kaymak, Emma L. Houlder, Syed Murtuza Baker, Ben R. Dickie, Louis Boon, Joanne E. Konkel, Matthew R. Hepworth, Andrew S. MacDonald, Gwendalyn J. Randolph, Dominik Rückerl, Judith Allen, T helper 2 cells control monocyte to tissue-resident macrophage differentiation during nematode infection of the pleural cavity, Immunity, 2023, Journal Article, PUBLISHED  DOI
Tachó-Piñot R, Stamper CT, King JI, Matei-Rascu V, Richardson E, Li Z, Roberts LB, Bassett JW, Melo-Gonzalez F, Fiancette R, Lin IH, Dent A, Harada Y, Finlay C, Mjösberg J, Withers DR, Hepworth MR., Bcl6 is a subset-defining transcription factor of lymphoid tissue inducer-like ILC3., Cell reports, 42, (11), 2023, p113425 , Journal Article, PUBLISHED  DOI
Caitlin M. McManus, Tiffany Bouchery, Mona Suleiman, Anna O. Kildemoes, Annabel Ferguson, Tao Wang, Conor M. Finlay, Ryan Chan, Tess Renahan, Ananya Mukundan, Gyaviira Nkurunungi, Sarah D. Bobardt, Hydra 2022: return of the interactive conference on helminth parasitology after the pandemic, Trends in Parasitology, 2022, Journal Article, PUBLISHED  DOI
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, PUBLISHED  DOI  URL
Fiancette R, Finlay CM, Willis C, Bevington SL, Soley J, Ng STH, Baker SM, Andrews S, Hepworth MR, Withers DR., Reciprocal transcription factor networks govern tissue-resident ILC3 subset function and identity., Nature immunology, 22, (10), 2021, p1245-1255 , Journal Article, PUBLISHED  DOI
  

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Animal Models of ANCA Vasculitis in, editor(s)Aman Sharma , Textbook of Systemic Vasculitis 2nd Edition, 2023, [Conor M Finlay, Mark A Little], Book Chapter, PUBLISHED
CP McEntee, S Houston, CM Finlay, S Rossi, G Liu, TN Shaw, J Casulli, M Fife, C Smedley, View ORCID ProfileTS Griffith, View ORCID ProfileM Pepper, T Hussell, PM Hansbro, View ORCID ProfileJ-M Schwartz, H Paidassi, MA Travis, A subset of CD4+ effector memory T cells limit immunity to pulmonary viral infection and prevent tissue pathology via activation of latent TGFß, BioRxiv, (2023.03.02.527395), 2023, Journal Article, PUBLISHED

  


Award Date
Best presentation from selected abstracts - Irish Society of Immunology 2019
Visiting student training scheme - Weizmann Institute of Science 2015
Valdicotrian - Biochemistry with Immunology degree 2007
Best Undergraduate Research Poster Prize - School of Biochemistry and Immunology 2007
TBSI Post-Doc Research Day - Runner up talk prize 2015
Wiley Top Cited Article Award - Parasite Immunology 2022
EFIS/EJI Travel/Abstract Award Winners Presenting at Cytokines 2021 2021
I am a Cellular Immunologist and bioinformatician who combines molecular, in vivo and translational research. My main reserach interest is in the differentiation and function of monocnuclear phagocytes (monocytes, macrophages and dendritic cells) in tissues during inflammation. I am particularly interested in how classically inflammatory "Type 1" immune responses and anti-inflammatory "Type 2" immmune response affect the differentiation paths that macrophages take in tissues. To study these concepts in diseases of two organs, the Kidney and the pleural cavity. I have a long-term interests in cell-cell interactions during infection and autoimmunity, particularly in how T cells instuct myeloid cells like macrophages, neutrophils, eosinophils and mast cells.