Meduni Vienna: New insights into the development of allergic asthma
A research team from MedUni Vienna has gained new insights into the role of the immune system in allergic asthma. The study examined the molecular regulation of certain immune cells, known as pathogenic Th2 cells, which are involved in the development of allergic diseases and are responsible for persistent inflammation of the respiratory tract. The results, which have been published in the journal Nature Communications, could help to develop new treatments for allergic asthma.
The research project, led by Nicole Boucheron and Matarr Khan at the Institute of Immunology at the Center for Pathophysiology, Infectiology and Immunology at MedUni Vienna, involved studies on pathogenic Th2 cells in a mouse model of house dust mite allergy. T helper 2 cells (Th2 cells for short) play an important role in the defence against parasites and support wound healing. In some cases, however, they react excessively to harmless common substances, such as the faeces of house dust mites. This leads to chronic inflammation, which can trigger or exacerbate severe illnesses such as allergic asthma. In the course of the study, the researchers were able to identify and better define subgroups of these pathogenic Th2 cells in the lungs. As their analyses showed, some Th2 cells trigger particularly strong inflammation by activating other immune cells (in particular eosinophils). These Th2 cells are also called pathogenic effector Th2 cells. Others remain in the lungs for long periods and can cause the disease to persist even when there is no direct contact with the allergen. These Th2 cells are called Th2 tissue-resident memory cells.
Targeted way to stop excessive immune responses
The molecular regulation of pathogenic effector Th2 cells and Th2 tissue-resident memory cells was examined in more detail in the study. The research team found that a central mechanism involves the enzyme histone deacetylase 1 (HDAC1). This enzyme helps control which genes are active in a cell. In healthy cells, HDAC1 ensures that pro-inflammatory chemical messengers (eg cytokines) are not produced in excessive amounts. The study revealed that HDAC1 was also important for the development of pathogenic Th2 cells. Inflammatory reactions in the lungs trigger processes in the cells that switch off HDAC1. This results in an uncontrolled immune response that drives inflammation. "These findings have direct implications for future treatment strategies," explains study leader Nicole Boucheron. Drugs that inhibit histone deacetylases are already used clinically for other medical conditions. However, the study shows clearly that they are not suitable for people with allergic asthma because they could worsen the disease. "Future therapies must target the pathogenic Th2 cells to stop the excessive response without weakening the immune system," adds first author Matarr Khan.
House dust mites are among the most common triggers of allergic diseases. According to estimates, up to 130 million people worldwide are affected. Allergic asthma is particularly severe, with airway inflammation that can severely restrict breathing. "Our findings lead to a better understanding of the mechanisms behind this disease and could help future development of targeted therapies for allergies," the study authors say.
Contact
Mag. Johannes Angerer
Medizinische Universität Wien
Leiter Kommunikation und Öffentlichkeitsarbeit
Telefon: 01/40160-11501
E-Mail: presse@meduniwien.ac.at
Website: https://www.meduniwien.ac.at/pr
Mag.a Karin Kirschbichler
Medizinische Universität Wien
Kommunikation und Öffentlichkeitsarbeit
Tel.: 01/ 40 160-11505
E-Mail: presse@meduniwien.ac.at
Website: https://www.meduniwien.ac.at/pr