“…Our results, however, complement findings of normal chemotactic response of psoriatic PMNL to LTB4 [22,23], suggesting that the accumulation of PMNL in psoriatic skin may be the result of an excess of cutaneous chemoattractant, rather than reflecting the increased readiness of psoriatic PMNL to migrate towards a che motactic stimulus. Indeed, elevated cuta neous levels of the chemoattractant eicosanoids LTB4 and 12-HETE were identified in psoriasis and atopic eczema [1][2][3]24], In addition, enhanced 5-lipoxygenase activity was found in skin of psoriatic patients [25] although peripheral PMNL of these patients display normal 5-lipoxygenase activity [15]. Thus, it is likely that elevated cutaneous lev els of chemoattractant eicosanoids may play a role in the initiation of the inflammatory infiltrate in both dermatoses, and that eico sanoids released from infiltrating inflamma tory cells may contribute to the maintenance of the inflammatory infiltrate and the hyper proliferation observed in chronic inflamma tory skin diseases [7], On the other hand, the altered responsiveness of monocytes from patients with psoriasis and atopic eczema towards LTB4 as demonstrated by Czarnetzki [26] leaves open the question of possi ble abnormalities of LTB4 receptors on cell types other than PMNL.…”