The accumulation of white blood cells is a hallmark of inflammation. The penetra tion through the vessel walls and the infiltration around the inflammatory stimulus is a complex process which involves active adherence and directed migration of the inflammatory cells. Chemotactic factors stimulate both adherence and migration. Technical tools such as the Boyden chamber [1] made it possible to study leukocyte migration in vitro. This technique allows differentiation between migration direct ed towards a chemotactic stimulus and non-directed migration. Until a decade ago only two naturally occurring molecules had been clearly iden tified as potent chemotactic attractants of neutrophilic granulocytes. They were the split product of the fifth complement component C5a [2] and the arachidonic acid metabolite leukotriene B4 [3]. In 1986, a novel human monocyte-derived chemo taxin attracting neutrophilic granulocytes with a similar potency was found [4]. This report was quickly confirmed by several groups [5-8]. The new factor was purified, cloned and sequenced [9, 10]. The term "interleukin 8" (IL-8) replaced the various names proposed previously [4-8]. Sequence data revealed that IL-8 belonged to a large family of chemotactic cytokines, now called "chemokines" [11]. Four subfamilies were distinguished on the basis of the number and position of the first cysteine residues. They are desig nated accordingly as C, CC, CXC and CX C chemokines [11-13]. The number of 3 human chemokines identified so far is close to 40 [11-13].
