Polymorphonuclear neutrophils (PMNs), comprising about two-thirds of peripheral blood leukocytes, are absent from uninfected, uninjured, ‘healthy' tissues. PMNs, proposed to be terminally differentiated and transcriptionally inactive, are the first cells to migrate to the site of infection to perform phagocytosis and to release cytotoxic compounds. Recent data reveal that PMNs actively acquire antigens, transcribe and express the genes for MHC class I and class II molecules, co-stimulatory molecules and several functionally diverse cytokines and chemokines that induce T-cell migration and differentiation. Thus, PMNs act not only as phagocytic scavengers and non-specific effectors of the innate immune system but also as significant inducers of T-dependent immune responses by processing and presenting antigens to T-cells in infectious and autoimmune diseases.