Kim Midwood
BSc (Hons), PhD
Professor of Matrix Biology
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..
Key publications
-
Tenascin-C is an endogenous activator of Toll-like receptor 4 that is essential for maintaining inflammation in arthritic joint disease.
Journal article
Midwood K. et al, (2009), Nat Med, 15, 774 - 780
-
Startups on the menu.
Journal article
Midwood K., (2013), Nat Biotechnol, 31
-
Distinct microenvironmental cues stimulate divergent TLR4-mediated signaling pathways in macrophages.
Journal article
Piccinini AM. et al, (2016), Sci Signal, 9
-
Endogenous control of immunity against infection: tenascin-C regulates TLR4-mediated inflammation via microRNA-155.
Journal article
Piccinini AM. and Midwood KS., (2012), Cell Rep, 2, 914 - 926
-
Identification of an immunodominant peptide from citrullinated tenascin-C as a major target for autoantibodies in rheumatoid arthritis.
Journal article
Schwenzer A. et al, (2016), Ann Rheum Dis, 75, 1876 - 1883
Recent publications
-
Alternative splicing controls cell lineage-specific responses to endogenous innate immune triggers within the extracellular matrix.
Journal article
Giblin SP. et al, (2020), Matrix Biol
-
Response to: 'Potential roles for tenascin in (very) early diagnosis and treatment of rheumatoid arthritis' by Cutolo et al.
Journal article
Aungier S. et al, (2020), Ann Rheum Dis, 79
-
Matrix-Targeting Immunotherapy Controls Tumor Growth and Spread by Switching Macrophage Phenotype.
Journal article
Deligne C. et al, (2020), Cancer Immunol Res, 8, 368 - 382
-
Treatment of severe periodontitis may improve clinical disease activity in otherwise treatment-refractory rheumatoid arthritis patients.
Journal article
Möller B. et al, (2020), Rheumatology (Oxford), 59, 243 - 245
-
Identification of TNFR2 and IL-33 as therapeutic targets in localized fibrosis.
Journal article
Izadi D. et al, (2019), Sci Adv, 5