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Acute inflammation is transiently activated by pathogens or tissue damage via TLRs/NF-B, leading to a burst of pro-inflammatory cytokines (e.g., IL-1, TNF-) to eliminate threats, followed by rapid resolution via anti-inflammatory signals (e.g., IL-10, TGF-) 18

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These alterations indicated a notable effect on the pattern of methylation associated with the regulatory regions of CADM1 and SOCS1