Väitös (lääketieteellinen mikrobiologia ja immunologia): MSc Inna Starskaia

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16.5.2025 klo 12.00 - 16.00
MSc Inna Starskaia esittää väitöskirjansa ”Early immune response in children developing type 1 diabetes” julkisesti tarkastettavaksi Turun yliopistossa perjantaina 16.5.2025 klo 12.00 (Vierailukeskus Joki, 2, kerros, Putous-auditorio, Turku).

Vastaväittäjänä toimii professori Katri Lindfors (Tampereen yliopisto) ja kustoksena professori Riitta Lahesmaa (Turun yliopisto). Tilaisuus on englanninkielinen. Väitöksen alana on lääketieteellinen mikrobiologia ja immunologia.

Väitöskirja yliopiston julkaisuarkistossa: https://urn.fi/URN:ISBN:978-952-02-0117-3 (kopioi linkki selaimeen).

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Tiivistelmä väitöstutkimuksesta:

Type 1 diabetes (T1D) is the most common chronic endocrine disorder in children. The disease is characterized by insulin deficiency due to immune cells destroying pancreatic beta cells that produce this hormone. Over the past few decades, there has been an increase in the incidence rate of T1D worldwide, with Finland reporting the highest rate. Currently, the appearance of autoantibodies against beta cells in the serum (so-called seroconversion) is the earliest and only indicator to predict T1D progression before its symptomatic onset. Early detection of the disease process is needed as it will allow timely intervention to prevent T1D development.

The first aim of this dissertation was to explore immune responses in children who later develop T1D at the very early stage of disease development, before seroconversion. This work reveals previously unknown early epigenetic changes in circulating immune cells associated with the disease, which might be useful for predicting T1D.

Another key aspect is the considerable heterogeneity in the rate of progression to T1D, depending on factors such as the age of seroconversion and the type of first-appearing autoantibody. Increasing knowledge in the pathogenesis of T1D leads to the recognition of different disease pathways behind one clinical disease. In this work, we identified changes in circulating immune cells associated with the type of autoantibody that appears first. This finding contributes to our understanding of the different pathogenic mechanisms underlying T1D and provides the possibility for disease prediction and prevention.

Furthermore, newly diagnosed patients with T1D are highly heterogeneous in the rate of disease progression. The large variation in T1D across individuals hampers the development of effective therapies. This work found that gene expression changes during the first year after clinical T1D onset can predict the rate of disease progression. The predictive model allowed us to divide patients into rapid and slow progressors. Clearly, the ability to classify patients would enable effective clinical trials and more personalized therapies in the future.

In conclusion, results of this dissertation indicate immune changes at the very early stage of T1D development and define means to identify distinct subsets of disease.
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