Inflammation is a critical immune response triggered by innate immune cells upon detecting infection or tissue injury. Pattern recognition receptors (PRRs) on the cell surface and in the cytoplasm recognize pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), leading to the activation of transcription factors such as NF-κB, AP1, CREB, c/EBP, and IRF. This activation promotes the expression of genes encoding enzymes, chemokines, cytokines, adhesion molecules, and regulators of the extracellular matrix, which are essential for recruiting and activating leukocytes to eliminate foreign particles and host debris. Some PRRs activate caspase-1, leading to the maturation of cytokines IL1β and IL18. Cell adhesion molecules and chemokines facilitate leukocyte extravasation, with chemokines stimulating G-protein-coupled receptors (GPCRs) to regulate leukocyte motility and effector functions. Allergens form antibody complexes that stimulate Fc receptors on mast cells, contributing to inflammation. While inflammation is essential for resolving infection and injury, chronic inflammation is a risk factor for cancer. PRRs include Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and Nod-like receptors (NLRs). TLRs recognize extracellular and endolysosomal PAMPs and DAMPs, triggering signaling pathways that activate NF-κB and MAPKs. TLR3, TLR7, and TLR9 also induce type I interferons. RLRs detect cytoplasmic viral and bacterial nucleic acids, leading to the activation of IRF3 and IRF7. NLRs, such as NOD1, NOD2, and NLRP3, recognize bacterial peptidoglycan and DAMPs, activating inflammasomes that lead to the processing and secretion of IL1β and IL18. The pro-inflammatory cytokine TNF promotes leukocyte recruitment and activation, and its signaling pathways involve NF-κB and MAPK activation. GPCRs, integrins, selectins, and Fc receptors also play roles in inflammation, with GPCRs mediating responses to lipid-based mediators and chemokines. Fc receptors, such as FcεRI and FcγRIIB, are involved in allergic reactions and phagocytosis. Inflammation is a risk factor for cancer, as persistent infections and chronic inflammation can lead to genetic mutations and tumor development. Inflammatory signaling pathways, such as those involving NF-κB and MAPKs, promote tumor growth and survival. However, inflammation alone is not sufficient for tumor development, and carcinogen-induced mutations are necessary. The complexity of inflammatory signaling pathways, including post-translational modifications like ubiquitylation, continues to be studied to understand their roles in immune responses and disease.Inflammation is a critical immune response triggered by innate immune cells upon detecting infection or tissue injury. Pattern recognition receptors (PRRs) on the cell surface and in the cytoplasm recognize pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), leading to the activation of transcription factors such as NF-κB, AP1, CREB, c/EBP, and IRF. This activation promotes the expression of genes encoding enzymes, chemokines, cytokines, adhesion molecules, and regulators of the extracellular matrix, which are essential for recruiting and activating leukocytes to eliminate foreign particles and host debris. Some PRRs activate caspase-1, leading to the maturation of cytokines IL1β and IL18. Cell adhesion molecules and chemokines facilitate leukocyte extravasation, with chemokines stimulating G-protein-coupled receptors (GPCRs) to regulate leukocyte motility and effector functions. Allergens form antibody complexes that stimulate Fc receptors on mast cells, contributing to inflammation. While inflammation is essential for resolving infection and injury, chronic inflammation is a risk factor for cancer. PRRs include Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and Nod-like receptors (NLRs). TLRs recognize extracellular and endolysosomal PAMPs and DAMPs, triggering signaling pathways that activate NF-κB and MAPKs. TLR3, TLR7, and TLR9 also induce type I interferons. RLRs detect cytoplasmic viral and bacterial nucleic acids, leading to the activation of IRF3 and IRF7. NLRs, such as NOD1, NOD2, and NLRP3, recognize bacterial peptidoglycan and DAMPs, activating inflammasomes that lead to the processing and secretion of IL1β and IL18. The pro-inflammatory cytokine TNF promotes leukocyte recruitment and activation, and its signaling pathways involve NF-κB and MAPK activation. GPCRs, integrins, selectins, and Fc receptors also play roles in inflammation, with GPCRs mediating responses to lipid-based mediators and chemokines. Fc receptors, such as FcεRI and FcγRIIB, are involved in allergic reactions and phagocytosis. Inflammation is a risk factor for cancer, as persistent infections and chronic inflammation can lead to genetic mutations and tumor development. Inflammatory signaling pathways, such as those involving NF-κB and MAPKs, promote tumor growth and survival. However, inflammation alone is not sufficient for tumor development, and carcinogen-induced mutations are necessary. The complexity of inflammatory signaling pathways, including post-translational modifications like ubiquitylation, continues to be studied to understand their roles in immune responses and disease.