Human CCL4 (C-C motif chemokine ligand 4, also known as MIP-1β, macrophage inflammatory protein-1 beta) is a pro-inflammatory chemokine that plays a key role in immune cell recruitment and regulation of inflammatory and antiviral immune responses. CCL4 primarily signals through the CCR5 receptor, promoting chemotaxis of monocytes, macrophages, dendritic cells, natural killer (NK) cells, and activated T lymphocytes to sites of infection, inflammation, or tissue injury. In humans, CCL4 is produced by activated macrophages, dendritic cells, T lymphocytes, epithelial cells, and endothelial cells following stimulation by microbial products or inflammatory cytokines such as TNF-α and IL-1β. CCL4 contributes to host defense by coordinating leukocyte trafficking and enhancing immune activation during infections; it is also involved in viral immunity, particularly in HIV infection, where CCL4 competes with the virus for the CCR5 co-receptor, thereby inhibiting viral entry into target cells. Dysregulated CCL4 expression is associated with chronic inflammatory and autoimmune diseases, including rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease, as well as cancer, where chemokine-mediated immune cell infiltration can influence tumor microenvironment dynamics. Because of its central role in immune cell migration and CCR5-mediated signaling, human CCL4 is widely studied as a biomarker of inflammation and a potential therapeutic target in infectious disease, immune-mediated disorders, and cancer immunology.