Monocytes, a subset of circulating white blood cells, play a crucial role in both homeostasis and inflammation. They originate from bone marrow progenitors and migrate to peripheral tissues, where they differentiate into macrophages or dendritic cells (DCs) in response to local growth factors, pro-inflammatory cytokines, and microbial products. Monocyte recruitment is essential for controlling infections and can also contribute to the pathogenesis of inflammatory and degenerative diseases. The mechanisms controlling monocyte trafficking under various conditions are being increasingly understood. Monocytes are divided into subsets based on chemokine receptor expression and surface molecule presence, such as LY6C and CD11b. CCR2, a chemokine receptor, is critical for the recruitment of inflammatory monocytes (LY6Chi monocytes) to sites of infection and inflammation. CX3CR1, another chemokine receptor, is involved in the patrolling behavior of low-lymphocyte-6 (LY6Clow) monocytes along endothelial cells. Monocyte recruitment is mediated by adhesion molecules like L-selectin, P-selectin, and E-selectin, which interact with specific ligands on endothelial cells. Monocytes can also traffic to non-inflamed tissues and replenish tissue-resident macrophages and DCs. During infections, monocytes and/or monocyte-derived cells can enter draining lymph nodes and promote adaptive immune responses. Studies in infectious disease models have revealed the mechanisms that mobilize and target monocytes to sites of microbial infection, including bacterial, protozoal, fungal, and viral infections. Monocyte recruitment is also involved in sterile inflammatory conditions like atherosclerosis. Understanding the mechanisms of monocyte recruitment can provide insights for developing new therapeutics to manipulate monocyte populations and enhance antimicrobial defense or dampen detrimental inflammation.Monocytes, a subset of circulating white blood cells, play a crucial role in both homeostasis and inflammation. They originate from bone marrow progenitors and migrate to peripheral tissues, where they differentiate into macrophages or dendritic cells (DCs) in response to local growth factors, pro-inflammatory cytokines, and microbial products. Monocyte recruitment is essential for controlling infections and can also contribute to the pathogenesis of inflammatory and degenerative diseases. The mechanisms controlling monocyte trafficking under various conditions are being increasingly understood. Monocytes are divided into subsets based on chemokine receptor expression and surface molecule presence, such as LY6C and CD11b. CCR2, a chemokine receptor, is critical for the recruitment of inflammatory monocytes (LY6Chi monocytes) to sites of infection and inflammation. CX3CR1, another chemokine receptor, is involved in the patrolling behavior of low-lymphocyte-6 (LY6Clow) monocytes along endothelial cells. Monocyte recruitment is mediated by adhesion molecules like L-selectin, P-selectin, and E-selectin, which interact with specific ligands on endothelial cells. Monocytes can also traffic to non-inflamed tissues and replenish tissue-resident macrophages and DCs. During infections, monocytes and/or monocyte-derived cells can enter draining lymph nodes and promote adaptive immune responses. Studies in infectious disease models have revealed the mechanisms that mobilize and target monocytes to sites of microbial infection, including bacterial, protozoal, fungal, and viral infections. Monocyte recruitment is also involved in sterile inflammatory conditions like atherosclerosis. Understanding the mechanisms of monocyte recruitment can provide insights for developing new therapeutics to manipulate monocyte populations and enhance antimicrobial defense or dampen detrimental inflammation.