Malin Flodström Tullberg

Malin Flodström Tullberg

Professor
Telephone: +46852487625
Mobile phone: +46769474569
Visiting address: Alfred Nobels allé 8, plan 7, 14152 Huddinge
Postal address: H7 Medicin, Huddinge, H7 CIM Flodström-Tullberg, 171 77 Stockholm
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About me

  • Malin Flodström Tullberg is Professor of Type 1 Diabetes at the Department of Medicine, Huddinge. Her research focuses on understanding the causes of the disease type 1 diabetes and contributing to the development and preclinical testing of new preventive measures against the disease. She also has an interest in the disese cystic fibrosis and mechanisms behind cystic fibrosis related diabetes and impaired antiviral defense mechanisms.

Research

  • Professor Flodström Tullberg’s research group has a central role in advancing our understanding of the etiology and pathogenesis of type 1 diabetes. Leveraging their unique expertise in both in vitro and in vivo models, the group has made groundbreaking discoveries regarding the intricate interactions between pancreatic islet cells, the immune system, and environmental factors (such as enteroviruses and the microbiome). The group has also produced and performed pre-clinical testing of new enterovirus vaccines. Recently, the group has also turned its attention to disease biomarkers, particularly non-invasive methods for detecting beta cell damage. Their robust platform for such studies positions them at the forefront of diabetes research. 

Articles

All other publications

Selected grants

  • A framework for production and testing next generation vaccines against non-polio enteroviruses
    Swedish Research Council
    1 January 2024 - 1 January 2026

Grants

  • Studies on pathogenesis and natural course in type 1 diabetes with implications for therapeutic interventions [Translated from Swedish by AI.]
    Swedish Child Diabetes Foundation
    1 January 2026
  • Early detection of type 1 diabetes – New microsampling and ultrasensitive detection of disease-predictive markers [Translated from Swedish by AI.]
    Trygg-Hansas Forskningsstiftelse
    2 September 2025
  • Studies on the Pathogenesis and Natural History of Type 1 Diabetes with Implications for Therapeutic Intervention
    Diabetesfonden – Stiftelsen Svenska Diabetesförbundets Forskningsfond
    1 January 2025 - 1 January 2027
  • Precision Proteome Monitoring in Microsampled Blood for Biomarker Discovery and Type 1 Diabetes Prevention: An AI-Driven Approach
    Novo Nordisk Foundation
    1 October 2024 - 30 September 2027
  • CFTR Modulator Treatment and New Vaccines for Intervention and Prevention of Lung Disease in Cystic Fibrosis
    Hjärt-Lungfonden (Swedish Heart-Lung Foundation)
    1 January 2024 - 1 January 2026
  • 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.

Employments

  • Professor, Diabetes Type 1, Department of Medicine, Huddinge, Karolinska Institutet, 2015-

Degrees and Education

  • Docent, Karolinska Institutet, 2005

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