Immune-Mediated Mechanisms driving brain repair and regeneration

The central nervous system (CNS) includes the brain and the spinal cord. Its immune functions are fulfilled by microglial cells, which are a specific population of macrophages. These cells have multiple roles related to physiology and pathology. As their specific functions are still poorly understood, however, the development of new strategies intended to modulate the microglia for therapeutic purposes requires more knowledge of their biology.

In order to investigate these questions, Valérie Wittamer’s laboratory uses the zebrafish as an experimental model, as it offers new opportunities for the study of functional aspects of the microglia. The zebrafish embryo is transparent, which, in conjunction with well-established transgenesis techniques, is a unique advantage when studying the development and behaviour of microglial cells in a non-invasive way in a vertebrate organism.

In addition, in the adult zebrafish—whose ability to regenerate is much higher than that of mammals—, earlier studies suggest a positive contribution of neuroinflammation during neural regeneration following brain damage. These observations point to the immune system, and very likely the microglia, as a key player in controlling these processes.

The project’s goal is to fully characterize the contribution of these cells to the cell regeneration process; it uses new zebrafish lines that have microglial deficiency, combined with advanced cellular, molecular, genetic, and imaging approaches.

Researchers expect to identify new mechanisms that enable the immune system to promote the regeneration of the damaged brain. The experiments planned as part of this project should also provide insight into the differences in the inflammation repair processes of zebrafish and mammals. Ultimately, it may open new perspectives in the field of neuroimmunology.

Coordination : Valérie Wittamer, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire (IRIBHM), Faculté de Médecine


Created on September 4, 2020