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Infection drives meningeal engraftment by inflammatory monocytes that impairs CNS immunity
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Infection drives meningeal engraftment by inflammatory monocytes that impairs CNS immunity
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Journal Article
Infection drives meningeal engraftment by inflammatory monocytes that impairs CNS immunity
2019
Overview
Tissue macrophages have an embryonic origin and can be replenished in some tissues under steady-state conditions by blood monocytes. However, little is known about the residency and properties of infiltrating monocytes after an inflammatory challenge. The meninges of the central nervous system (CNS) are populated by a dense network of macrophages that act as resident immune sentinels. Here we show that, following lymphocytic choriomeningitis virus infection, resident meningeal macrophages (MMs) acquired viral antigen and interacted directly with infiltrating cytotoxic T lymphocytes, which led to macrophage depletion. Concurrently, the meninges were infiltrated by inflammatory monocytes that engrafted the meningeal niche and remained in situ for months after viral clearance. This engraftment led to interferon-γ-dependent functional changes in the pool of MMs, including loss of bacterial and immunoregulatory sensors. Collectively, these data indicate that peripheral monocytes can engraft the meninges after an inflammatory challenge, imprinting the compartment with long-term defects in immune function.
The central nervous system meninges have a dense network of yolk sac–derived macrophages that serve a sentinel role. McGavern and colleagues show that this meningeal niche is replenished by bone marrow–derived inflammatory monocytes, which alters meningeal immune reactions after subsequent immune challenge.
Publisher
Nature Publishing Group US,Nature Publishing Group
