Flagship projects

Identifying the inflammatory messengers responsible for muscle damage

Role of interleukins in muscle dysfunction in myasthenia gravis

The project explores the role of certain interleukins produced directly in the muscle of patients with myasthenia gravis. These molecules, which are normally involved in tissue repair, appear to persist abnormally and could contribute to the muscle dysfunction seen in the disease.

Scientific challenge

In myasthenia gravis, the main mechanism is well understood: autoantibodies disrupt communication between the nerve and the muscle. The muscle itself, however, shows inflammatory abnormalities that remain poorly understood. Understanding how these local signals impair muscle function could shed light not only on myasthenia gravis, but also on other autoimmune diseases and on situations where muscle repair is ineffective.

Key questions to unravel

The work aims to determine:

which muscle cells produce these interleukins, in particular interleukin-17;
where they are produced within the tissue;
how they influence surrounding cells and contribute to muscle weakness or to impaired repair.

The aim is to identify the local mechanisms that worsen the disease and could become more precise therapeutic targets.

Scientific and methodological approach

The researchers will analyse:

patient muscle biopsies, already available in the collections of the Institute of Myology;
experimental models that make it possible to test the effect of interleukins on muscle fibres.

They will study the cell types present in the muscle, the inflammatory molecules these cells produce and the interactions between them. This work relies on close collaboration between researchers, engineers, clinicians and students.

In myasthenia gravis, certain inflammatory messengers amplify the damage and disrupt the proper functioning of muscle fibres. Muscle is like a mountain, with valleys and peaks, and our aim is to understand how the different features of the landscape communicate with one another and which mechanisms do the most to upset that balance. By identifying these signals and the cells that produce them, we are seeking to better understand the disease and what could open the way to better-suited treatments.
Nadine Dragin, researcher at the Center of Research in Myology

Expected impact on research and clinical practice

A better understanding of local inflammationRéaction non spécifique suscitée par un agent pathogène. could:

explain why some patients recover less well;
point towards more targeted treatments, acting on specific mechanisms rather than on the immune system as a whole;
allow the repurposing of existing drugs;
contribute to more personalised care, with fewer side effects.

This knowledge could also shed light on other settings where muscle struggles to repair itself, such as ageing or certain autoimmune diseases.