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IL-1 is generated by Kupffer cells through TLR4 stimulation but not by TLR9- or TLR3-dependent mechanisms124
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In addition, increasing neutrophils may contribute to the progression of AS through phagocytosis, ROS production damaging tissue and impairing endothelial function, repairing damaged tissues, restricting NET production, or directly releasing NET to counter inflammation, which may be beneficial for the progression of AS (32, 61, 203)
