Tolerization to pro-inflammatory signals

Tolerization to pro-inflammatory signals refers to the phenomenon where immune cells, especially macrophages, monocytes, and dendritic cells, become less responsive or actively suppress pro-inflammatory gene expression following repeated or chronic stimulation by inflammatory mediators such as Toll-like receptor (TLR) ligands (e.g., LPS). Molecular mechanisms behind this process include negative regulation of signaling pathways (NF-κB p50 homodimers, BCL-3), epigenetic modifications, and increased transcription of anti-inflammatory genes. This process is critical for limiting tissue damage during ongoing infection or inflammation, but overactivation can result in unwanted immune suppression and vulnerability to infection or cancer[1][2][3][5].

Other names

Endotoxin toleranceTLR toleranceinflammation tolerance

Immunosuppressive drugs may disrupt or modulate development of tolerized states in immune cells Interferons and various cytokines may modulate transition between pro-inflammatory activation and tolerance[1][2][5][6]