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Kim Midwood

Kim Midwood, PhD 

Professor of Matrix Biology

Kennedy Institute of Rheumatology,
Nuffield Department of Orthopaedics,
Rheumatology and Musculoskeletal Sciences,
University of Oxford, 
Roosevelt Drive, Headington,

Present Position

  • Professor  


  • British Society for Matrix Biology 


  • New Investigator Award, Medical Research Council (2007-2012)
  • Award for Outstanding Achievement in Research (Nature Journals, 2009)
  • Senior Research Fellowship, Arthritis Research UK (2012 - present)
  • Mover and shaker: top 50 women in Biobusiness (2015)
  • Honorary Secretary, British Society for Matrix Biology (2016 - present)

Editorial Boards 

  • Guest Editor for Cell Adhesion and Migration (2013)
  • American Journal of Cell Physiology (2013-2016)
  • Matrix Biology (2013 - present)
  • International Journal of Experimental Pathology (2016 – present)

Research Themes 

  • Professor Kim Midwood graduated with a B.Sc. (HONS) in Biochemistry from Edinburgh University in 1995. She completed her Ph.D. in the Department of Pathology at Edinburgh University in 1999, focusing on how changes in the extracellular matrix affect cellular signalling pathways in arthritis.
    She undertook postdoctoral training in the lab of Professor Jean Schwarzbauer, at Princeton University from 1999, continuing her work investigating the molecular mechanisms by which the cellular environment defines cell phenotype.
    In 2004 she established the Matrix Immunology group in the Kennedy Institute of Rheumatology at Imperial College London, moving to Oxford University in 2011. In 2007 she won an MRC New Investigators Award and in 2012 an Arthritis Research UK Senior Fellowship. She founded the BioTech company Nascient Ltd in 2012.
    The Midwood group has a long-standing interest in defining the molecular mechanisms underlying a successful immune response and understanding how these are compromised in related diseases.  Our research focuses on investigating how extracellular matrix molecules that are specifically induced upon tissue damage and infection control cell behaviour during inflammation and repair.
    Combining structural, biochemical, proteomic, genomic and computational approaches, we investigate how matrix molecules create a 3D, pro-inflammatory niche at sites of inflammation enabling cells to proliferate and thrive, how this specialized microenvironment persists in inflammatory diseases, driving chronic inflammation and how this information can be translated into new therapeutic strategies.
    For more information please visit our webpages:

Selected Research Publications 

  • Zuliani-Alvarez L, Marzeda AM, Deligne C, Schwenzer A, McCann FE, Marsden BD, Piccinini AM, Midwood KS. (2017)
    Mapping tenascin-C interaction with toll-like receptor 4 reveals a new subset of endogenous inflammatory triggers.
    Nat Communications; 8(1):1595.
  • Schwenzer A, Quirke AM, Marzeda AM, Wong A, Montgomery AB, Sayles HR, Eick S, Gawron K, Chomyszyn-Gajewska M, Łazarz-Bartyzel K, Davis S, Potempa J, Kessler BM, Fischer R, Venables PJ, Payne JB, Mikuls TR, Midwood KS. (2017)
    Association of Distinct Fine Specificities of Anti-Citrullinated Peptide Antibodies With Elevated Immune Responses to Prevotella intermedia in a Subgroup of Patients With Rheumatoid Arthritis and Periodontitis.
    Arthritis Rheumatol. 69(12):2303-2313.
  • Midwood KS, Chiquet M, Tucker RP, Orend G (2016)
    Tenascin-C at a glance.
    J Cell Sci. 2016 Dec 1;129(23):4321-4327
  • Aungier, S. and Midwood, K.S. (2106)
    The Extracellular Matrix: a new dimension in disease diagnosis and treatment.
    The Biochemist.
  • Piccinini, A.M., Zuliani-Alvarez, L., Lim, J.M.P and Midwood, K.S. (2016)
    Distinct microenvironmental cues trigger divergent TLR4-mediated immune signalling in macrophages.
    Science Signalling Aug 30;9(443):ra86.
  • Schwenzer, A., Jiang, X., Mikuls, T.R., Payne, J.B., Sayles, H.R., Quirke, A.M., Kessler, B.M., Fischer, R., Venables, P.J., Lundberg, K. and Midwood, K.S. (2016)
    Identification of an immunodominant peptide from citrullinated tenascin-C as a major target for autoantibodies in rheumatoid arthritis.
    Ann Rheum Dis. 75(10):1876-83
  • Midwood, K.S. (2013)
    Startups on the menu.
    Nat Biotechnol. 2013 Jun;31(6):490.
  • Piccinini, A.M. and Midwood, K.S. (2012)
    Endogenous Control of Immunity against Infection: tenascin-C regulates TLR4 mediated inflammation via microRNA-155.
    Cell Reports 2 (4): 914-926.
  • To, W.S. and Midwood, K.S. (2011)
    Identification of novel and distinct binding sites within tenascin-C for soluble and fibrillar fibronectin.
    J. Biol. Chem. 286 (17) 14881-14891. (Paper of the week with accompanying editorial piece)
  • To, W.S. and Midwood, K.S. (2010)
    Cryptic domains of tenascin-C differentially control fibronectin fibrillogenesis.
    Matrix Biol. 29, 573-585.
  • Midwood, K.S., Sacre, S., Piccinini, A.M. Inglis, J., Trebaul, A., Chan, E.K., Drexler, S., Kashiwagi, M., Orend, G., Brennan, F., and Foxwell, B (2009).
    Tenascin-C is an endogenous activator of TLR4 that promotes the maintenance of inflammation in arthritic joint disease.
    Nature Medicine. 15(7), 774-80.