The role of group 2 innate lymphoid cells producing GM-CSF in homeostasis and inflammation

• Grant number: 24/07534-5
• Support Opportunities: Scholarships abroad - Research Internship - Doctorate
• Start date: October 31, 2024
• End date: October 30, 2025
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Thiago Mattar Cunha
• Grantee: Gabriel Victor Lucena da Silva
• Supervisor: Burkhard Becher
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Institution abroad: University of Zurich (UZH), Switzerland
• Associated to the scholarship: 21/10494-7 - Importance of IL-33 in the development of Wallerian degeneration and its actions on immune cells, BP.DR

Abstract

Once considered passive anatomical barriers, the meninges have emerged as an important regulatory niche for immune responses in the central nervous system. Recent studies have revealed that the meninges harbor various lymphoid and myeloid cells. Among this large repertoire of immune cells, type 2 innate lymphoid cells (ILC2s) stand out for their fundamental role in modulating local processes. ILC2s, which do not have antigen receptors, respond to cytokines and contribute directly to immune defense and tissue repair. The expression of surface markers, including CD127 and ST2, ensures a specific phenotype, as well as localization and responsiveness to stimuli. In particular, ILC2s produce granulocyte and macrophage colony-stimulating factors, influencing the activation of dendritic cells and macrophages, as well as promoting inflammation. Understanding the intricate function of ILC2s, especially their cytokine production and interaction with GM-CSF, sheds light on their importance in both the homeostasis and pathology of the CNS and border tissues. Here, we will investigate the role of ILC2s and their derived GM-CSF in meningeal immunity. Using mouse fate mapping approaches and complementary techniques, we will characterize meningeal ILC2, identify the impact of GM-CSF deletion on ILC2 in the meninges, and evaluate how ILC2-derived GM-CSF may contribute to meningeal immunity and hematopoiesis.