Tohtorinhattu lääketiede (3)

Väitös (immunologia): MSc Rahul Biradar

Aika

29.5.2026 klo 12.00 – 16.00

MSc Rahul Biradar esittää väitöskirjansa ”Gene regulation of human T cells: Regulation of T cell differentiation and changes in T cells during progression of type 1 diabetes” julkisesti tarkastettavaksi Turun yliopistossa perjantaina 29.5.2026 klo 12.00 (Turun yliopisto, Medisiina D, Alhopuro-sali, Kiinamyllynkatu 10, Turku).

Vastaväittäjänä toimii professori, tohtori Lucy Walker (University college London, Iso-Britannia) ja kustoksena professori, tohtori Riitta Lahesmaa (Turun yliopisto ja Åbo Akademi). Tilaisuus on englanninkielinen. Väitöksen alana on immunologia.

Tiivistelmä väitöstutkimuksesta:

The human immune system relies on many coordinated cell types to defend us from infections. Immune cells can recognize invading microbes and protect our health, but sometimes this system becomes misdirected. When immune cells attack the body’s own tissues, autoimmune diseases such as rheumatoid arthritis, psoriasis, multiple sclerosis, inflammatory bowel disease, and type 1 diabetes can develop.

Type 1 diabetes occurs when immune cells destroy the insulin producing cells of the pancreas. The first clinical sign of the disease is the appearance of diabetes related autoantibodies in the blood, but important immune changes begin much earlier. Understanding these earliest events is essential for finding ways to delay or even prevent the disease.


My dissertation focuses on CD4⁺ T cells, a central group of immune cells that guide and regulate immune responses. When they encounter a pathogen, these cells develop into specialized “T helper” (Th) subsets that perform specific tasks. By studying CD4⁺ T cells at single cell resolution in children who later developed type 1 diabetes, my research identifies early changes in particular T cell subsets that arise before autoantibodies appear. This is a key finding as it reveals the earliest detectable immune alterations that may trigger the autoimmune process.

The dissertation also investigates a T helper subset called Th17 cells, which are involved in several autoimmune diseases. My research identifies two proteins—FOSL1 and FOSL2—as molecular regulators that influence how Th17 cells develop and function. In addition, the study discovered a previously unknown enhancer region within the RORA gene that helps control Th17 cell differentiation. This provides new information about how gene regulation shapes the behavior of immune cells that drive autoimmunity.

Together, these findings offer important insight into how specialized immune cells become dysregulated and contribute to autoimmune diseases. The broader impact of this research is that it brings us closer to detecting type 1 diabetes risk earlier, understanding how harmful immune responses begin, and ultimately developing therapies that could intervene before the disease fully develops.

Viestintä