Monocytes play a crucial role in the immune response to microbial pathogens, both directly and by differentiating into macrophages and dendritic cells (DCs). In humans and mice, monocytes are divided into two major subsets: inflammatory monocytes (Ly6C+ monocytes) and resident monocytes (CX3CR1+ monocytes). Inflammatory monocytes respond rapidly to microbial stimuli, secrete cytokines and antimicrobial factors, and traffic to sites of infection via CCR2-mediated chemokine signaling. Murine models show that CCR2-mediated monocyte recruitment is essential for defense against *Listeria monocytogenes*, *Mycobacterium tuberculosis*, *Toxoplasma gondii*, and *Cryptococcus neoformans*. Recent studies highlight the complexity of monocyte recruitment, involving CCR2-mediated emigration from the bone marrow to the bloodstream and subsequent trafficking into infected tissues. The mechanisms that promote chemokine secretion, monocyte differentiation, and trafficking, and ultimately monocyte-mediated microbial killing remain active areas of investigation. Monocytes also contribute to the regulation of adaptive immune responses, with both positive and negative effects on T cell proliferation and differentiation. Chemokines, particularly MCP-1 (CCL2), play a pivotal role in monocyte recruitment during infection, but other chemokines and receptors may also be involved.Monocytes play a crucial role in the immune response to microbial pathogens, both directly and by differentiating into macrophages and dendritic cells (DCs). In humans and mice, monocytes are divided into two major subsets: inflammatory monocytes (Ly6C+ monocytes) and resident monocytes (CX3CR1+ monocytes). Inflammatory monocytes respond rapidly to microbial stimuli, secrete cytokines and antimicrobial factors, and traffic to sites of infection via CCR2-mediated chemokine signaling. Murine models show that CCR2-mediated monocyte recruitment is essential for defense against *Listeria monocytogenes*, *Mycobacterium tuberculosis*, *Toxoplasma gondii*, and *Cryptococcus neoformans*. Recent studies highlight the complexity of monocyte recruitment, involving CCR2-mediated emigration from the bone marrow to the bloodstream and subsequent trafficking into infected tissues. The mechanisms that promote chemokine secretion, monocyte differentiation, and trafficking, and ultimately monocyte-mediated microbial killing remain active areas of investigation. Monocytes also contribute to the regulation of adaptive immune responses, with both positive and negative effects on T cell proliferation and differentiation. Chemokines, particularly MCP-1 (CCL2), play a pivotal role in monocyte recruitment during infection, but other chemokines and receptors may also be involved.