Salmonella infection induces the reorganization of follicular dendritic cell networks concomitant with the failure to generate germinal centers.
Marcial-Juárez, Edith ; Pérez-Toledo, Marisol ; Nayar, Saba ; Pipi, Elena ; Alshayea, Areej ; Persaud, Ruby ; Jossi, Sian E ; Lamerton, Rachel ; Barone, Francesca ; Henderson, Ian R ... show 1 more
Marcial-Juárez, Edith
Pérez-Toledo, Marisol
Nayar, Saba
Pipi, Elena
Alshayea, Areej
Persaud, Ruby
Jossi, Sian E
Lamerton, Rachel
Barone, Francesca
Henderson, Ian R
Abstract
Germinal centers (GCs) are sites where plasma and memory B cells form to generate high-affinity, Ig class-switched antibodies. Specialized stromal cells called follicular dendritic cells (FDCs) are essential for GC formation. During systemic Salmonella Typhimurium (STm) infection GCs are absent, whereas extensive extrafollicular and switched antibody responses are maintained. The mechanisms that underpin the absence of GC formation are incompletely understood. Here, we demonstrate that STm induces a reversible disruption of niches within the splenic microenvironment, including the T and B cell compartments and the marginal zone. Alongside these effects after infection, mature FDC networks are strikingly absent, whereas immature FDC precursors, including marginal sinus pre-FDCs (MadCAM-1+) and perivascular pre-FDCs (PDGFRβ+) are enriched. As normal FDC networks re-establish, extensive GCs become detectable throughout the spleen. Therefore, the reorganization of FDC networks and the loss of GC responses are key, parallel features of systemic STm infections.
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Date
2023-03-02
Type
Article
Subject
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Citation
Marcial-Juárez E, Pérez-Toledo M, Nayar S, Pipi E, Alshayea A, Persaud R, Jossi SE, Lamerton R, Barone F, Henderson IR, Cunningham AF. Salmonella infection induces the reorganization of follicular dendritic cell networks concomitant with the failure to generate germinal centers. iScience. 2023 Mar 2;26(4):106310. doi: 10.1016/j.isci.2023.106310
Journal / Source Title
iScience
DOI
10.1016/j.isci.2023.106310
PMID
36950118
Publisher
Cell Press
Publisher’s URL
http://www.cell.com/iscience/home
