Academic Publication IL-1R signaling drives enteric glia-macrophage interactions in colorectal cancer
Research Abstract & Technology Focus
Enteric glia have been recently recognized as key components of the colonic tumor microenvironment indicating their potential role in colorectal cancer pathogenesis. Although enteric glia modulate immune responses in other intestinal diseases, their interaction with the colorectal cancer immune cell compartment remains unclear. Through a combination of single-cell and bulk RNA-sequencing, both in murine models and patients, here we find that enteric glia acquire an immunomodulatory phenotype by bi-directional communication with tumor-infiltrating monocytes. The latter direct a reactive enteric glial cell phenotypic and functional switch via glial IL-1R signaling. In turn, tumor glia promote monocyte differentiation towards pro-tumorigenic SPP1
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tumor-associated macrophages by IL-6 release. Enteric glia cell abundancy correlates with worse disease outcomes in preclinical models and colorectal cancer patients. Thereby, our study reveals a neuroimmune interaction between enteric glia and tumor-associated macrophages in the colorectal tumor microenvironment, providing insights into colorectal cancer pathogenesis.
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What is the core focus of the research titled 'IL-1R signaling drives enteric glia-macrophage interactions in colorectal cancer'?
This literature focuses on: Abstract Enteric glia have been recently recognized as key components of the colonic tumor microenvironment indicating their potential role in colorectal cancer pathogenesis. Although enteric glia modulate im...
What other academic literature is closely related to 'IL-1R signaling drives enteric glia-macrophage interactions in colorectal cancer'?
Yes, highly correlated activity was mapped. An entry titled 'Targeting of TAMs: can we be more clever than cancer cells?' discusses this: АbstractWith increasing incidence and geography, cancer is one of the leading causes of death, reduced quality of life and disability worldwide. Pr...
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