Mural cells interact with macrophages in the dura mater to regulate CNS immune surveillance.

Autor:	Min H; Marcus Center for Cellular Cures, Duke University School of Medicine, Durham, NC, USA.; Department of Neurosurgery, Duke University School of Medicine, Durham, NC, USA., O'Neil SM; Marcus Center for Cellular Cures, Duke University School of Medicine, Durham, NC, USA., Xu L; Marcus Center for Cellular Cures, Duke University School of Medicine, Durham, NC, USA., Moseman EA; Department of Integrative Immunobiology, Duke University School of Medicine, Durham, NC, USA., Kurtzberg J; Marcus Center for Cellular Cures, Duke University School of Medicine, Durham, NC, USA.; Department of Pediatrics, Duke University School of Medicine, Durham, NC, USA., Filiano AJ; Marcus Center for Cellular Cures, Duke University School of Medicine, Durham, NC, USA.; Department of Neurosurgery, Duke University School of Medicine, Durham, NC, USA.; Department of Integrative Immunobiology, Duke University School of Medicine, Durham, NC, USA.; Department of Pathology, Duke University School of Medicine, Durham, NC, USA.
Jazyk:	angličtina
Zdroj:	The Journal of experimental medicine [J Exp Med] 2024 Feb 05; Vol. 221 (2). Date of Electronic Publication: 2024 Jan 09.
DOI:	10.1084/jem.20230326
Abstrakt:	The central nervous system (CNS) tightly regulates access of circulating immune cells. Immunosurveillance is therefore managed in the meninges at the borders of the CNS. Here, we demonstrated that mural cells, which include pericytes and smooth muscle cells, decreased coverage around blood vessels in the dura, the outermost layer of the meninges, and upregulated gene pathways involved in leukocyte migration in presymptomatic experimental autoimmune encephalomyelitis (EAE). Partially depleting mural cells promoted the trafficking of CNS antigen-specific T cells to the dura in a process that depended on resident antigen-presenting cells, thereby increasing susceptibility to passive EAE. Mechanistically, mural cells physically contacted macrophages in the dura and transferred cytoplasmic components, including processing bodies (RNA granules shown to reprogram transcriptomes), which were critical to suppress antigen-dependent T helper (TH) cell activation and TH17 differentiation. Our study revealed a mechanism by which mural cell-macrophage interactions regulate the trafficking of CNS antigen-specific T cells to the dura. (© 2024 Min et al.)
Databáze:	MEDLINE
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