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Inflammation during the Th1 tissue-damaging immune response of MIRS. Blood clots generate ischemia, which causes necrosis. Released DAMPs induce neutrophil and monocyte activation trough TLR and inflammasome activation, which in turn potentiate Th1 polarization. Inflammatory monocytes mature and become M1 macrophages. Tissue damage amplification comes in the form of NETs, granule components, and ROS produced by innate cells and direct complement attack.
