Monocytes originate from bone marrow progenitors and travel through the bloodstream to peripheral tissues. During homeostasis and inflammation, they migrate to tissues where they differentiate into macrophages or dendritic cells after being conditioned by local factors. Monocytes are essential for controlling infections but also contribute to inflammatory diseases. This review discusses the mechanisms of monocyte trafficking under different conditions. Monocytes are divided into subsets based on chemokine receptor expression. In mice, LY6C high monocytes express high levels of CCR2 and low levels of CX3CR1, while LY6C low monocytes express high levels of CX3CR1 and low levels of CCR2. These subsets have distinct roles in immune responses. CCR2 is crucial for the recruitment of LY6C high monocytes to sites of inflammation. CCL2 and CCL7, which bind to CCR2, are important for monocyte recruitment during infections. The CX3CL1-CX3CR1 axis is important for the patrolling of LY6C low monocytes along endothelial cells. CCR1 and CCR5 also play roles in monocyte recruitment, with CCR5 being involved in atherosclerosis and multiple sclerosis. CCR6, CCR7, CCR8, and CXCR2 are also involved in monocyte recruitment, though less studied. Adhesion molecules are critical for monocyte trafficking, with integrins and other adhesion molecules facilitating rolling, adhesion, and transmigration. Monocytes patrol blood vessels and enter tissues, with LY6C high monocytes being recruited to sites of inflammation. Monocyte recruitment is essential for immune defense and tissue repair, but excessive recruitment can worsen inflammation. Monocytes contribute to the development of tissue macrophages and dendritic cells. In infections, monocytes are recruited to infected tissues and mediate direct antimicrobial activity. Monocyte subsets have different roles in immune responses, with LY6C high monocytes being important for early recruitment and LY6C low monocytes for patrolling. In bacterial infections, monocytes are recruited to the liver and spleen, where they contribute to immune defense. CCR2 deficiency reduces monocyte recruitment and worsens infection. In fungal infections, monocytes are important for immune defense, with CCR2 deficiency leading to reduced monocyte recruitment and increased susceptibility. In viral infections, monocytes are recruited to the liver and brain, where they contribute to immune defense. CCR2 deficiency reduces monocyte recruitment and worsens viral clearance. In sterile inflammation, monocytes contribute to aseptic inflammatory conditions, with CCR2 playing a role in monocyte recruitment. Monocyte recruitment is regulated by chemokines and adhesion molecules, with CCR2 being crucial for monocyte egress from the bone marrow. Bone marrow stromal cells, such as mesenchymal stem cells and CAR cells, produce CCL2 in response to microbial molecules, promoting monMonocytes originate from bone marrow progenitors and travel through the bloodstream to peripheral tissues. During homeostasis and inflammation, they migrate to tissues where they differentiate into macrophages or dendritic cells after being conditioned by local factors. Monocytes are essential for controlling infections but also contribute to inflammatory diseases. This review discusses the mechanisms of monocyte trafficking under different conditions. Monocytes are divided into subsets based on chemokine receptor expression. In mice, LY6C high monocytes express high levels of CCR2 and low levels of CX3CR1, while LY6C low monocytes express high levels of CX3CR1 and low levels of CCR2. These subsets have distinct roles in immune responses. CCR2 is crucial for the recruitment of LY6C high monocytes to sites of inflammation. CCL2 and CCL7, which bind to CCR2, are important for monocyte recruitment during infections. The CX3CL1-CX3CR1 axis is important for the patrolling of LY6C low monocytes along endothelial cells. CCR1 and CCR5 also play roles in monocyte recruitment, with CCR5 being involved in atherosclerosis and multiple sclerosis. CCR6, CCR7, CCR8, and CXCR2 are also involved in monocyte recruitment, though less studied. Adhesion molecules are critical for monocyte trafficking, with integrins and other adhesion molecules facilitating rolling, adhesion, and transmigration. Monocytes patrol blood vessels and enter tissues, with LY6C high monocytes being recruited to sites of inflammation. Monocyte recruitment is essential for immune defense and tissue repair, but excessive recruitment can worsen inflammation. Monocytes contribute to the development of tissue macrophages and dendritic cells. In infections, monocytes are recruited to infected tissues and mediate direct antimicrobial activity. Monocyte subsets have different roles in immune responses, with LY6C high monocytes being important for early recruitment and LY6C low monocytes for patrolling. In bacterial infections, monocytes are recruited to the liver and spleen, where they contribute to immune defense. CCR2 deficiency reduces monocyte recruitment and worsens infection. In fungal infections, monocytes are important for immune defense, with CCR2 deficiency leading to reduced monocyte recruitment and increased susceptibility. In viral infections, monocytes are recruited to the liver and brain, where they contribute to immune defense. CCR2 deficiency reduces monocyte recruitment and worsens viral clearance. In sterile inflammation, monocytes contribute to aseptic inflammatory conditions, with CCR2 playing a role in monocyte recruitment. Monocyte recruitment is regulated by chemokines and adhesion molecules, with CCR2 being crucial for monocyte egress from the bone marrow. Bone marrow stromal cells, such as mesenchymal stem cells and CAR cells, produce CCL2 in response to microbial molecules, promoting mon