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Kiss, Máté; Lebegge, Els; Murgaski, Aleksandar; Van Damme, Helena; Kancheva, Daliya; Brughmans, Jan; Scheyltjens, Isabelle; Talebi, Ali; Awad, Robin Maximilian; Elkrim, Yvon; Bardet, Pauline M. R.; Arnouk, Sana M.; Goyvaerts, Cleo; Swinnen, Johan; Nana, Frank Aboubakar; Van Ginderachter, Jo A.; Laoui, Damya

Junctional adhesion molecule-A is dispensable for myeloid cell recruitment and diversification in the tumor microenvironment

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  • Media type: E-Article
  • Title: Junctional adhesion molecule-A is dispensable for myeloid cell recruitment and diversification in the tumor microenvironment
  • Contributor: Kiss, Máté; Lebegge, Els; Murgaski, Aleksandar; Van Damme, Helena; Kancheva, Daliya; Brughmans, Jan; Scheyltjens, Isabelle; Talebi, Ali; Awad, Robin Maximilian; Elkrim, Yvon; Bardet, Pauline M. R.; Arnouk, Sana M.; Goyvaerts, Cleo; Swinnen, Johan; Nana, Frank Aboubakar; Van Ginderachter, Jo A.; Laoui, Damya
  • Published: Frontiers Media SA, 2022
  • Published in: Frontiers in Immunology, 13 (2022)
  • Language: Not determined
  • DOI: 10.3389/fimmu.2022.1003975
  • ISSN: 1664-3224
  • Origination:
  • Footnote:
  • Description: 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.
  • Access State: Open Access