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Polymorphnuclear neutrophils (PMN) possess a very short half-life in the circulation because they constitutively undergo apoptosis (Gasmi et al., 1996; Stringer et al., 1996; Moulding et al., 1998). Under certain conditions PMN play an important role in the effectors arm of host immune defense through the clearance of immune complexes, the phagocytosis of opsonized particles, and the release of inflammatory mediators (Shen et al., 1987; Petroni et al., 1988; Lloyd et al., 1992). During the recent years the image of PMN has changed considerably. Traditionally considered to be the first line defense against bacterial infection. It became increasingly clear that PMN also participate in chronic inflammatory disease and regulation of the immune response when appropriately activated (Iking-Konert et al., 2002). Persistent Staphylococcus aureus-mediated local infection induces the local activation and transdifferentiation of PMN to cells with dendritic-like characteristics (Wagner et al., 2006).

Human Leukocyte Antigen Class II in Stimulated Polymorphnuclear Neutrophils