Research group Helena Erlandsson Harris
Translational research on inflammatory mechanisms active during juvenile idiopathic arthritis to develop better diagnostic and prognostic tools and new therapy. We have a specific interest in the alarmin HMGB1.
Around 1500-2000 swedish children have chronic joint inflammation, juvenile idiopathic arthritis (JIA). There is a great need for improved diagnostic and prognostics tools as well as new therapeutic options. In addition to joint inflammation, destruction of joint tissue and pain are hallmarks of the disease. An improved, in depth understanding of the molecular mechanisms driving these three hallmarks forms the basis for development of diagnostic/prognostic biomarker tests as well as development of new, subgroup specific therapy – precision medicine.
Alarmins is a class of endogenous molecules released from stressed, injured and dying cells with the function to initiate an inflammatory response. The protein HMGB1, a prototypic alarmin, is a nuclear protein during tissue homeostasis which when released can induce cell migration, cytokine production, cell differentiation and regeneration. All important features of the inflammatory response. Our research has clearly demonstrated HMGB1 as a mediator of inflammation. In arthritis, HMGB1 mediates inflammation, destruction and pain. Treatment targeting HMGB1 improves all three arthritis hallmarks.
Our projects are focused on expanding the molecular knowledge of the immune mechanisms active in JIA as a basis for biomarker and therapy development. To achieve this we analyse biosamples collected from children with JIA, our sample collection JABBA, and compare generated data with information retrieved from the national quality register Svenska barnreumaregistret. In a recently started project we are investigating the possible connection of JIA, neuroinflammation and its potential influence on quality of life.
How HMGB1 is contributing to inflammation, pan and destruction is studied with a translational approach using molecular and cellular functional studies, analyses of HMGB1 in patient samples and model systems.
To develop better diagnostics, prognostics and treatment for JIA. Our results will also be applicable for many other inflammatory diseases.
Research group leader
Cecilia Aulin, PhD, senior forskare
Erik Sundberg, MD, PhD, senior forskare
Henna Salo, doktorand
Rebecka Heinbäck, doktorand
Heshuang Qu, doktorand
Karina Mördrup, forskningssköterska
Disulfide and Fully Reduced HMGB1 Induce Different Macrophage Polarization and Migration Patterns.
Salo H, Qu H, Mitsiou D, Aucott H, Han J, Zhang XM, Aulin C, Erlandsson Harris H
Biomolecules 2021 05;11(6):
Juvenile idiopathic arthritis patients have a distinct cartilage and bone biomarker profile that differs from healthy and knee-injured children.
Struglics A, Saleh R, Sundberg E, Olsson M, Erlandsson Harris H, Aulin C
Clin Exp Rheumatol ;38(2):355-365
Cleavage of HMGB1 by Proteolytic Enzymes Associated with Inflammatory Conditions.
Sowinska A, Rensing M, Klevenvall L, Neog M, Lundbäck P, Harris HE
Front Immunol 2020 ;11():448262
A novel high mobility group box 1 neutralizing chimeric antibody attenuates drug-induced liver injury and postinjury inflammation in mice.
Lundbäck P, Lea JD, Sowinska A, Ottosson L, Fürst CM, Steen J, Aulin C, Clarke JI, Kipar A, Klevenvall L, Yang H, Palmblad K, Park BK, Tracey KJ, Blom AM, Andersson U, Antoine DJ, Erlandsson Harris H
Hepatology 2016 11;64(5):1699-1710
Therapeutic administration of etoposide coincides with reduced systemic HMGB1 levels in macrophage activation syndrome.
Palmblad K, Schierbeck H, Sundberg E, Horne AC, Erlandsson Harris H, Henter JI, Andersson U
Mol Med 2021 05;27(1):48