ArticleThe Journal of clinical investigation2023
Discovering the fibroblastic reticular cell in the immune tumor microenvironment in lymphoma.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Multiplexed imaging mass cytometry elicits p-S6 as a therapeutic and prognostic factor in diffuse large B-cell lymphoma.Blood advances · 2025Article
- Orbital fibroblastic reticular cell tumor: A case report and literature review for a rare disease.Medicine · 2025Review
- Abnormal proportions and functions of myeloid-derived suppressor cells in peripheral blood of patients with diffuse large B-cell lymphoma.BMC cancer · 2025Article
- An off-target effect of class A CpG-oligonucleotides on suppressing the cyclic GMP-AMP synthase signaling in fibroblastic reticular cells.Frontiers in pharmacology · 2025Article
- Exploring the Potential of Enhanced Prognostic Performance of NCCN-IPI in Diffuse Large B-Cell Lymphoma by Integrating Tumor Microenvironment Markers: Stromal FOXC1 and Tumor pERK1/2 Expression.Cancer medicine · 2024Article
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Abstract
The study of the cellular and molecular microenvironment in B cell lymphoma, especially diffuse large B cell lymphoma (DLBCL), has led to prognostic and therapeutic algorithms that may improve patient outcomes. Emerging gene signature panels provide a granular understanding of DLBCL based on the immune tumor microenvironment (iTME). In addition, some gene signatures identify lymphomas that are more responsive to immune-based treatment, indicating that the iTME has a biological signature that could affect outcomes when targeted. In this issue of the JCI, Apollonio et al. report on fibroblastic reticular cells (FRCs) as potential targets in aggressive lymphoma. FRCs interacted with lymphoma cells and induced a state of chronic inflammation that suppressed immune function by impeding optimal T cell migration and inhibiting CD8+ T cell lytic function. These findings suggest that manipulating the iTME by directly targeting FRCs may enhance responses to immunotherapy in DLBCL.
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