ArticleScientific reports2024
Absence of sympathetic innervation hampers the generation of tertiary lymphoid structures upon acute lung inflammation.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Artery Tertiary Lymphoid Organs Form Neuroimmune Cardiovascular Interfaces in Atherosclerosis.Immunological reviews · 2026Review
- Tertiary Lymphoid Structures Across Organs: Context, Composition, and Clinical Levers.Immunological reviews · 2025Review
- The Sunrise of Tertiary Lymphoid Structures in Cancer.Immunological reviews · 2025Review
- Neuroimmune Interactions and Their Role in Immune Cell Trafficking in Cardiovascular Diseases and Cancer.International journal of molecular sciences · 2025Review
- Nerves, nodes, and neoplasia.Frontiers in immunology · 2025Review
- Tertiary lymphoid structures in anticancer immunity.Nature reviews. Cancer · 2024Review
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Authors and funding
7 authors.
Funding
Abstract
Tertiary lymphoid structures (TLS) are lymphoid organs present in inflammatory non-lymphoid tissues. Studies have linked TLS to favorable outcomes for patients with cancers or infectious diseases, but the mechanisms underlying their formation are not fully understood. In particular, secondary lymphoid organs innervation raises the question of sympathetic nerve fibers involvement in TLS organogenesis. We established a model of pulmonary inflammation based on 5 daily intranasal instillations of lipopolysaccharide (LPS) in immunocompetent mice. In this setting, lung lymphoid aggregates formed transiently, evolving toward mature TLS and disappearing when inflammation resolved. Sympathetic nerve fibers were then depleted using 6-hydroxydopamine. TLS quantification by immunohistochemistry showed a decrease in LPS-induced TLS number and surface in denervated mouse lungs. Although a reduction in alveolar space was observed, it did not impair overall pulmonary content of transcripts encoding TNF-α, IL-1β and IFN-γ inflammation molecules whose expression was induced by LPS instillations. Immunofluorescence analysis of immune infiltrates in lungs of LPS-treated mice showed a drop in the proportion of CD23
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Registered trials
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