EMAP II is an antiangiogenic and proinflammatory cytokine (expressed by microglia/macrophages). EMAP II appears to be a profound modulator of inflammatory reactions of the innate immune system and might participate in a variety of pathogenic immune-processes in the mammalian brain. EMAP II is a potential mediator of inflammatory responses in autoimmunity and a considered target to stage reactions of monocytic lineage cells in inflammatory reactions. In normal tissues EMAP II is expressed in endocrine organs, in cells of neuroendocrine origin, but also in tissues with high cell turnover. Under pathophysiological conditions EMAP II has several functions. It triggers the recruitment of macrophages by elevating cytosolic-free Ca2+ concentrations, it stimulates leukocyte chemotaxis, it induces the expression of TNF-alpha and tissue factor (TF) by monocytes and myeloperoxidase (MPO) by polymorphonuclear cells (PNMs). Furthermore it stimulates the release of von Willebrand-factor, P- and E-selectin by endothelial cells and EMAP II induces endothelial programmed cell death in vitro.