Inflammation is triggered by innate immune cells detecting infection or tissue injury through pattern recognition receptors (PRRs) on the cell surface and in the cytoplasm. PRRs respond to pathogen-associated molecular patterns (PAMPs) or host-derived damage-associated molecular patterns (DAMPs), activating transcription factors like NF-κB, AP1, CREB, c/EBP, and IRF. This activation induces the expression of genes encoding enzymes, chemokines, cytokines, adhesion molecules, and extracellular matrix regulators, promoting leukocyte recruitment and activation. A subset of PRRs activates caspase-1, leading to the maturation of cytokines IL1β and IL18. Cell adhesion molecules and chemokines facilitate leukocyte extravasation, while G-protein-coupled receptors (GPCRs) mediate signals that regulate leukocyte motility and effector functions. Allergens can also trigger inflammation by forming antibody complexes that stimulate Fc receptors on mast cells. Chronic inflammation is increasingly recognized as a risk factor for cancer, with persistent infections and inflammatory conditions linked to certain cancers. The role of posttranslational modifications, such as ubiquitylation, in these pathways is still being elucidated, and understanding how innate immune cells integrate signals from multiple inflammatory mediators is crucial for therapeutic interventions in inflammatory disorders.Inflammation is triggered by innate immune cells detecting infection or tissue injury through pattern recognition receptors (PRRs) on the cell surface and in the cytoplasm. PRRs respond to pathogen-associated molecular patterns (PAMPs) or host-derived damage-associated molecular patterns (DAMPs), activating transcription factors like NF-κB, AP1, CREB, c/EBP, and IRF. This activation induces the expression of genes encoding enzymes, chemokines, cytokines, adhesion molecules, and extracellular matrix regulators, promoting leukocyte recruitment and activation. A subset of PRRs activates caspase-1, leading to the maturation of cytokines IL1β and IL18. Cell adhesion molecules and chemokines facilitate leukocyte extravasation, while G-protein-coupled receptors (GPCRs) mediate signals that regulate leukocyte motility and effector functions. Allergens can also trigger inflammation by forming antibody complexes that stimulate Fc receptors on mast cells. Chronic inflammation is increasingly recognized as a risk factor for cancer, with persistent infections and inflammatory conditions linked to certain cancers. The role of posttranslational modifications, such as ubiquitylation, in these pathways is still being elucidated, and understanding how innate immune cells integrate signals from multiple inflammatory mediators is crucial for therapeutic interventions in inflammatory disorders.