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Dr. Thomas Mark Conlon Ph.D.

Team Leader Research Group Immunopathology of COPD, LHI

My vision is that by targeting the immune system we can modulate tissue repair and regeneration to ultimately develop novel therapeutic targets to reverse chronic lung disease – particularly COPD, the third leading cause of death worldwide.

My vision is that by targeting the immune system we can modulate tissue repair and regeneration to ultimately develop novel therapeutic targets to reverse chronic lung disease – particularly COPD, the third leading cause of death worldwide.

Academic career and research areas

Thomas “Tom” Conlon completed his PhD in 2005 at the Cambridge Institute for Medical Research and Department of Pathology at the University of Cambridge elucidating the transcriptional regulation of immunoglobulin gene diversification particularly somatic hypermutation, mechanisms underpinning the core function of adaptive B cell immunity. Favouring a translational application to his research, he moved to the University of Cambridge’s Department of Surgery for the next seven years to investigate the interaction of T and B cells in chronic allograft rejection, working with heterotopic heart transplant models. Here he elucidated the role of graft versus host and auto-immune reactions in chronic allograft rejection and the importance of Lymphotoxin driven tertiary lymphoid organ development and the function of T follicular helper cells in the chronic rejection of heart allografts.

           

In 2013 to further strengthen his translational research aspirations, he joined the research group of Dr. Ali Önder Yildirim, at what is now the institute of Lung Health and Immunity (Directed by Dr. Yildirim) of Helmholtz Munich, to investigate the immunopathogenesis of COPD. Tom is now a Team Leader in the same group, whose research is driven in two primary directions. Firstly, how is the immune system, particularly the adaptive immune system, modulating tissue injury in COPD and how can we reverse this process to turn back on endogenous regeneration mechanisms in the lung. This was elegantly exemplified in his recent landmark study published in Nature, where he demonstrated that the blockade of lymphotoxin signalling not only resolved tertiary lymphoid organs in the lungs but induced regeneration of lung tissue by re-activating endogenous WNT/β-catenin developmental pathways in alveolar epithelial cells and reversed disease progression. His second research stream is the role epigenetic regulation plays in the immunopathegenesis of COPD, particularly the role of the protein arginine methyl transferases (PRMTs). He recently demonstrated in Nature Commun. that PRMT7 mediated mono-methylation of histones at regulatory elements of RAP1A, was responsible for adhesion and migration of monocytes into the lungs of COPD patients.  

Skills

 COPDEpigenetics  Adaptive Immunity PRMTs  Innate Immunity

Professional Background

Since 2021

Group Leader “Immunopathology of COPD”, Comprehensive Pneumology Center (CPC), Helmholtz Zentrum Muenchen, Institute of Lung Biology and Disease; Munich, Germany

2013

Post-Doc, iLBD (LHI), Helmholtz Munich

2006

Post-Doc, Department of Surgery, University of Cambridge

2005

PhD, CIMR, University of Cambridge

Honors and Awards

  • 2022 International Travel Scholarship Award – ATS

  • 2018 Prize of Excellence in Lung Research – MLC and DZL symposium

  • 2017 UHU Seed Funding Award – UWA

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Publications

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2022 Scientific Article in Nature Communications

Günsel, G.G.# ; Conlon, T.M.# ; Jeridi, A.# ; Kim, R. ; Ertüz, Z. ; Lang, N.J. ; Ansari, M. ; Novikova, M. ; Jiang, D. ; Strunz, M. ; Gaianova, M. ; Hollauer, C. ; Gabriel, C. ; Angelidis, I. ; Doll, S. ; Pestoni, J. ; Edelmann, S.L. ; Kohlhepp, M.S. ; Guillot, A. ; Bassler, K. ; ... ; Ballester-Lopez, C. ; Genes Robles, C.M. ; Smirnova, N.F. ; Rehberg, M. ; Agarwal, C. ; Krikki, I. ; Stöger, T. ; Burgstaller, G. ; Heissmeyer, V. ; Rinkevich, Y. ; Schiller, H. B. ; Conrad, M. ; Schneider, R. ; Yildirim, A.Ö.

The arginine methyltransferase PRMT7 promotes extravasation of monocytes resulting in tissue injury in COPD.

2021 Nature

Conlon, T.M. ; John-Schuster, G. ; Heide, D. ; Pfister, D. ; Lehmann, M. ; Hu, Y. ; Ertüz, Z. ; ... ; Ansari, M. ; Strunz, M. ; Mayr, C. ; Angelidis, I. ; Costa, R. ; Güneş, G. ; Jeridi, A. ; Beroshvili, G. ; Alsafadi, H.N. ; Lindner, M. ; Burgstaller, G. ; Becker, L. ; Irmler, M. ; Stöger, T. ; Beckers, J. ; Wagner, D.E. ; Theis, F.J. ; Hrabě de Angelis, M. ; Schiller, H. B. ; Königshoff, M. ; Yildirim, A.Ö.

Publisher Correction: Inhibition of LTβR signalling activates WNT-induced regeneration in lung (Nature, (2020), 588, 7836, (151-156), 10.1038/s41586-020-2882-8).