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Fibroblastic niches in action: CCL19+ reticular cells drive anti-tumor immunity in lung cancer
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Fibroblastic niches in action: CCL19+ reticular cells drive anti-tumor immunity in lung cancer
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Journal Article
Fibroblastic niches in action: CCL19+ reticular cells drive anti-tumor immunity in lung cancer
2025
Overview
In a groundbreaking study published in Cell, Onder and colleagues revealed the pivotal role of fibroblastic reticular cells (FRCs) in creating specialized niches, providing robust immune activation against non-small cell lung cancer (NSCLC), which paves the way for innovative therapeutic strategies.1 Cancers are complex ecosystems comprising tumor cells intricately interwoven with a diverse array of non-cancerous cells—including immune cells, cancer-associated fibroblasts (CAFs), endothelial cells, and various tissue-specific resident cells—embedded within a remodeled extracellular matrix (ECM), collectively shaping the tumor microenvironment (TME).2 The TME differs markedly among tumors, influenced by factors such as tumor location, stage, the inherent properties of the cancer cells, and individual patient conditions. The TME plays a crucial role in cancer progression by regulating processes such as cancer cell migration, proliferation, tumor vascularization, and the modulation of anti-cancer immune responses.2 Effects of the TME are partially mediated by secreted factors, including exosomes, metabolites, cytokines, chemokines, and a remodeled extracellular matrix produced by CAFs, which profoundly influence cancer progression.2 Numerous studies revealed that the TME plays a pivotal role in modulating anti-cancer immune responses, either promoting or suppressing these processes in a manner that appears highly context-dependent.3 Effective immune responses against cancer cells basically involve three different key mechanisms. (i) tumor-antigen-specific CD8+ T cells are activated in draining lymph nodes and then (ii) recruited into the tumor. (iii) Recruited CD8+ T cells are maintained in an activated state within specialized niches in the TME.1 The TME controls these mechanisms through multiple pathways. [...]the TME’s physical and metabolic landscape may either facilitate or impede infiltration and survival of immune cells. The study underscores the pivotal role of Ccl19+ FRCs in enhancing T-cell effector functions within the TME in NSCLC and suggests that CD8+ T cells achieve full effector potential through their interactions with CCL19-expressing FRCs in the TME after initial activation and proliferation in draining lymph nodes.1 Remarkably, ablation of Ccl19+ FRCs in the lung substantially increases the tumor burden in xenograft models of lung cancer in immunized mice, underscoring the critical role of these cells for sustaining robust anti-cancer immune responses and slowing lung cancer progression (Fig. 1).1 In this work, the authors made substantial progress in uncovering the cellular origin of FRCs.
