Experimental study demonstrates that fibroblastic reticular cells maintain lymph node macrophages via CSF1 signaling in mouse and human tissue, highlighting a critical immune niche.
The lymph node (LN) is home to resident macrophage populations that are essential for immune function and homeostasis, but key factors controlling this niche are undefined. Here, we show that fibroblastic reticular cells (FRCs) are an essential component of the LN macrophage niche. Genetic ablation of FRCs caused rapid loss of macrophages and monocytes from LNs across two in vivo models. Macrophages co-localized with FRCs in human LNs, and murine single-cell RNA-sequencing revealed that FRC subsets broadly expressed master macrophage regulator CSF1. Functional assays containing purified FRCs and monocytes showed that CSF1R signaling was sufficient to support macrophage development. These effects were conserved between mouse and human systems. These data indicate an important role for FRCs in maintaining the LN parenchymal macrophage niche.
No takes yet. Share an insight, caveat, or question.
D’Rozario et al. (2023) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: