ArticleJournal of neuroinflammation2025
B cells are not drivers of stromal cell activation during acute CNS infection.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Tertiary lymphoid structures in renal cell carcinoma: from heterogeneity dissection to translational precision immunotherapy.Frontiers in immunology · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
backgroundCNS stromal cells, especially fibroblasts and endothelial cells, support leukocyte accumulation through upregulation of adhesion molecules and lymphoid chemokines. While chronically activated fibroblast networks can drive pathogenic immune cell aggregates known as tertiary lymphoid structures (TLS), early stromal cell activation during CNS infection can support anti-viral T cells. However, the cell types and factors driving early stromal cell activation is poorly explored.
aimsA neurotropic murine coronavirus (mCoV) infection model was used to better characterize signals that promote fibroblast networks supporting accumulation of antiviral lymphocytes. Based on the early appearance of IgD
resultsKinetic analysis of stromal cell activation in olfactory bulbs and brains revealed that upregulation of adhesion molecules and lymphoid chemokines Ccl19, Ccl21 and Cxcl13 closely tracked viral replication. Immunohistochemistry revealed that upregulation of the fibroblast marker podoplanin (PDPN) at meningeal and perivascular sites mirrored kinetics of RNA expression. Moreover, both B cells and T cells colocalized to areas of PDPN reactivity, supporting a potential role in regulating stromal cell activation. However, specific depletion of LTβ from B cells using Mb1-creERT2 x Ltβ
conclusionsNeither B cell-derived LTβ or B cells are primary drivers of stromal cell activation networks in the CNS following mCoV infection. Although supplementary agonist mediated LTβR engagement confirmed a role for LTβ in enhancing PDPN and lymphoid chemokine expression, it impeded T cell migration to the CNS parenchyma and viral control. Our data overall indicate that stromal cells can integrate LTβR signals to tune their activation, but that LTβ is not necessarily essential and can even dysregulate protective antiviral T cell functions.
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