Vad orsakar typ-1 diabetes och hur kan sjukdomen förhindras? – Malin Flodström Tullberg forskargrupp

I vår forskning strävar vi efter att förstå hur olika faktorer i vår omgivning så som virusinfektioner och den mikrobiologiska floran påverkar risken för typ-1 diabetes.

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Gruppbild på nio personer i inomhusmiljö.

Vår forskning

I vår forskning strävar vi efter att förstå hur olika faktorer i vår omgivning så som virusinfektioner och den mikrobiologiska floran påverkar risken för typ-1 diabetes. Vi arbetar även med att ta fram nya sätt med vilka sjukdomen kan förhindras.

Typ-1 diabetes eller som sjukdomen tidigare kallades, barndiabetes, uppstår då kroppens insulinproducerande celler förstörs. Detta leder till höga blodsockernivåer och kräver daglig insulinbehandling för resten av livet. Sjukdomen är den näst vanligaste kroniska sjukdomen hos barn. I Sverige är en av 200 personer drabbade.

Typ-1 diabetes är förknippat med allvarliga komplikationer. Exakt varför och hur de insulinproducerande cellerna skadas vet man inte, därför finns ingen behandling som motverkar att skadorna uppstår.

Mer information om forskningen i Malin Flodström-Tullbergs grupp finns på den engelska sidan.

Publikationer

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Finansiering

Forskningsbidrag

  • European Commission
    1 January 2024 - 31 December 2027
    ENT1DEP aims to define causal links between infections and NCDs by focusing on enterovirus (EV) infections and type 1 diabetes (T1D), a robust association without proof of causality. Causality is addressed by a multidisciplinary, multi-layer approach, using in-vitro and in-vivo models, unique human samples, and artificial intelligence to identify mechanisms and related biomarkers, asking 3 key questions: 1. Why are only insulin-producing β-cells destroyed by EVs? Weak β-cell antiviral responses and high expression of EV entry receptors may favour EV persistence. This hypothesis is addressed using human cell models (stem-cell-derived β/α-cells, organoids, their genetic modifications, anti-EV T-cells) and pancreas tissues from T1D patients. 2. Why do only some individuals develop T1D after EV infection? Weak EV immunity may predispose to virus spreading to pancreas, persistence and local inflammation, triggering autoimmunity. This hypothesis is addressed by analysing adaptive and innate immune responses to EVs, correlating these with gene polymorphisms and EV persistence in children followed from birth and who developed T1D. 3. How can EV-associated T1D risk be attenuated? By using vaccines inducing protective immunity and antiviral drugs eradicating persistent infection. This hypothesis is addressed by examining samples from pioneering EV vaccine and T1D antiviral trials to develop biomarkers of vaccine- vs infection-induced immunity as surrogates of vaccine efficacy
    by studying whether vaccine-induced antibodies prevent EV-induced diabetes in mice
    by correlating antiviral treatment with EV clearance and immunity to identify biomarkers for EV eradication and patient selection. The final goal is to identify individuals at risk for EV-induced T1D as targets for early interventions. These outcomes may also facilitate progress in other NCDs extending impact. This new knowledge is disseminated among stakeholders to facilitate optimal NCD prevention and treatment.
  • Swedish Research Council
    1 December 2023 - 30 November 2026
    Non-polio enteroviruses (NPEVs) are common pathogens with &gt
    280 virus serotypes that can infect humans. Examples of NPEVs include rhinoviruses, EV-D68 and EV71. NPEVs have major medical and socio-economic impact
    Rhinoviruses cause the common cold, which accounts for a large proportion of disease-related work absences. Other NPEVs are associated with severe diseases including polio-like disorders, cardiomyopathy, aseptic meningitis, and type 1 diabetes. Recent outbreaks of EV-D68 and EV71 have caused severe neurological disease and deaths. New NPEVs are likely to emerge in the coming years. Despite their propensity to cause large outbreaks leading to cases of severe disease, only one NPEV vaccine is available for clinical use and antivirals are not available. Thereby, preparedness for NPEV outbreaks and pandemics is poor. This novel and multidisciplinary research program will make a significant contribution in this area
    we use advanced technologies and rational design to produce and test 2nd generation VLP-based NPEV vaccines. By studying natural- and vaccine induced immunity via immunopeptidomics screens and in silico analyses, we will also generate critical information for vaccine efficacy testing and improvements of vaccine design. The project has a 3-year duration.  By establishing this powerful platform, our studies have a clear translational potential and will strongly contribute to better preparedness for future (re)emerging NPEV outbreaks and pandemics.

Medarbetare och kontakt

Gruppledare

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Postadress

Karolinska Institutet, Medicine Huddinge, Alfred Nobels Allé 8, Stockholm, SE14152, Sweden

Nyckelord:
Autoantikroppar Autoimmuna sjukdomar Biomarkörer Bukspottkörtel Cell- och molekylärbiologi Visa alla
Innehållsgranskare:
Malin Flodström Tullberg
Karin Vikström
2025-09-04