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CRC-infiltrating Th17 cells induced the expression of G-CSF by CAF leading to the recruitment to the TME of CD11b + Gr1 + myeloid cells endowed with pro-angiogenic features, and thus promoting resistance to VEGF blockade therapy (137)

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This heightened permeability facilitates the infiltration of immune cells to the infection site, but it also contributes to increased ROS production from both endothelial cells and the infiltrating immune cells

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