ArticleFrontiers in immunology2022
Junctional adhesion molecule-A is dispensable for myeloid cell recruitment and diversification in the tumor microenvironment.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- Pan-cancer single-cell atlases of mouse and human tumor-associated dendritic cells.Nature communications · 2026Article
- Epigenomic preconditioning of peripheral monocytes determines their transcriptional response to the tumor microenvironment.Genome medicine · 2025Article
- Intestinal neuron-associated macrophages in health and disease.Nature immunology · 2025Review
- Potentials and future perspectives of multi-target drugs in cancer treatment: the next generation anti-cancer agents.Cell communication and signaling : CCS · 2024Review
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Authors and funding
17 authors at 4 institutions in 1 country.
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Abstract
Junctional adhesion molecule-A (JAM-A), expressed on the surface of myeloid cells, is required for extravasation at sites of inflammation and may also modulate myeloid cell activation. Infiltration of myeloid cells is a common feature of tumors that drives disease progression, but the function of JAM-A in this phenomenon and its impact on tumor-infiltrating myeloid cells is little understood. Here we show that systemic cancer-associated inflammation in mice enhanced JAM-A expression selectively on circulating monocytes in an IL1β-dependent manner. Using myeloid-specific JAM-A-deficient mice, we found that JAM-A was dispensable for recruitment of monocytes and other myeloid cells to tumors, in contrast to its reported role in inflammation. Single-cell RNA sequencing revealed that loss of JAM-A did not influence the transcriptional reprogramming of myeloid cells in the tumor microenvironment. Overall, our results support the notion that cancer-associated inflammation can modulate the phenotype of circulating immune cells, and we demonstrate that tumors can bypass the requirement of JAM-A for myeloid cell recruitment and reprogramming.
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