A UWr expert on this year’s Nobel Prize in Medicine
We asked professor Ewa Marcinkowska from the Faculty of Biotechnology at the University of Wrocław – an expert conducting research at the interface of haematology and immunology, focusing on therapies inducing the maturation of blasts in acute myeloid leukaemia – to explain what the immune system is all about and why research into it is so demanding and multifaceted.
This year’s Nobel Prize in Physiology or Medicine has been awarded to Mary E. Brunkow and Fred Ramsdell (USA) and Shimon Sakaguchi (Japan). They have elucidated how the immune system functions — specifically, how it avoids attacking the body’s own cells.
Prof. Ewa Marcinkowska:
The main task of the immune system is to eliminate pathogens — that has long been known. This task is far from simple, so over the course of evolution, numerous mechanisms have developed that enable immune cells to distinguish between what is safe and what is potentially dangerous.
Some of these mechanisms involve recognising proteins and sugars typical of pathogens as distinct from those characteristic of humans. The carriers of these ‘hostile’ structures must be eliminated — this is the role of the cells of the innate immune system. But that alone is not enough.
To combat pathogens more precisely, adaptive immunity evolved — allowing T lymphocytes (helper and cytotoxic) and B lymphocytes to recognise and destroy billions of different structures that are ‘non-self’ and remove them.
However, if you think about it, fighting and eliminating cannot be the immune system’s only function. After all, it cannot attack the body’s own cells. That is why all T and B lymphocytes that could potentially target the body’s own tissues die — most often during embryonic development or childhood.
But the immune system must also refrain from attacking food, components of inhaled air, or so-called ‘good bacteria’ (commensals). This is a far more difficult task. It is performed by so-called regulatory T cells (Tregs). These were discovered in mice by Shimon Sakaguchi and his team in 1995 (Sakaguchi, S. et al., J Immunol 155(3), 1151–1164; 1995). They are few in number, and Sakaguchi distinguished them from other helper T cells by the presence of a surface protein called CD25. When this small population of lymphocytes was removed from mice, the animals developed autoimmune diseases and allergies.
A few years later, Mary Brunkow and Fred Ramsdell (with their team) discovered in mice that a gene called FoxP3 is essential for regulatory lymphocytes to function properly (Brunkow, M. et al., Nat Genet 27, 68–73; 2001). Unfortunately, this gene can be mutated in humans. Since FoxP3 is located on the X chromosome, women carrying the mutation usually show no symptoms, but carrier mothers can pass it on to their sons. Boys lack a second X chromosome with a healthy copy of the gene, and therefore suffer from a severe deficiency of functional FoxP3 protein, leading to serious autoimmune and allergic symptoms.
This discovery opened the door to further research. Today we know much more about regulatory lymphocytes. We also know that, in addition to them, the body is protected from autoimmunity by so-called immune checkpoints — the discovery for which the 2018 Nobel Prize was awarded.
Professor Ewa Marcinkowska, currently a member of the National Science Centre Council (NCN), has led research projects funded by the Committee for Scientific Research, the Ministry of Science and Higher Education, the National Science Centre, the 7th Framework Programme for Research, and Horizon Europe.
Text by Katarzyna Górowicz-Maćkiewicz
Date of publication: 7.10.2025
Added by: E.K.
