The Protein STAT3 Helps the Immune System Fight Leukemia

Study at the Karl Landsteiner University of Health Sciences uncovers unknown interaction between leukemic cells and immune cells. Potential biomarkers for future immunotherapies found.
By: PR&D
 
July 16, 2024 - PRLog -- Krems (Austria), 16 July 2024: The protein STAT3 helps the immune system to recognise leukemic cells. This interaction, which is important for future immunotherapies, is now understood in detail thanks to a study at the Karl Landsteiner University of Health Sciences (KL Krems). The study showed that STAT3 influences the formation of surface structures on leukemic cells that make them vulnerable to the immune system. If these structures are missing, leukemic cells can escape the body's innate immune surveillance. The expression of STAT3 in and the surface structures on leukemic cells could be a potential biomarker for future immunotherapies.

Acute myeloid leukemia (AML) is the second most common form of leukemia in children and the most common form in people over the age of 50. Despite good treatment options, almost half of the patients with AML relapse. Immunotherapies, which help the body's own immune system fight the remaining cancer cells, are seen as a promising approach to improving this relapse rate. Many clinical trials focus on natural killer cells (NK cells) - lymphocytes that kill virus-infected and tumour cells. However, AML cells are often able to evade the body's immune defence. Understanding the mechanisms responsible for this is of great importance for the success of immunotherapies. A team from KL Krems has made an important contribution to this research field, which has now been published in an international scientific journal.

Efficient Elimination

"We show for the first time how STAT3 improves the elimination of leukemic cells by NK cells," explains Prof. Dr Dagmar Stoiber-Sakaguchi, Head of the Division of Pharmacology at KL Krems and last author of the study. "This happens due to an interaction with surface structures of the AML cells called ICAM-1. Indeed, the team was able to show that AML cells without STAT3 were less efficiently eliminated by NK cells - and also had less ICAM-1. ICAM-1 – Intercellular Adhesion Molecule 1 – serves as a binding site for patrolling NK cells, which is necessary for the destruction of cancer cells. If there is less ICAM-1, the NK cells cannot do their job properly.

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Location:Austria
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