Activated monocytes produce a variety of cytokines that are involved in inflammation, such as IL-1, TNF, chemotactic factors, transforming growth factor R, platelet-derived growth factor, and IFN-a and -Q (1). Chemotactic factors released at foci of injury or bacterial invasion are thought to mediate directed migration of leukocytes into inflammatory sites. Since the leukocyte composition of the inflammatory infiltrate depends on the temporal stage of the lesion (2) and the nature of the stimulus (3), it follows that some chemoattractants should be specific for a given type of leukocyte. We recently showed that LPS-stimulated monocytes produce a chemotactic factor that attracts neutrophils, but not monocytes (4). We purified this factor to homogeneity and described the N1-12-terminal sequence of the first 42 amino acids (5). We now report molecular cloning and sequencing ofthe full-length cDNA for this monocyte-derived neutrophil chemotactic factor (MDNCF)' and the deduced amino acid sequence of the entire molecule. Specific cDNA probes also enabled us to test the capacity of a number of cytokines to induce MDNCF mRNA expression in human PBMC. The stimulation of MDNCF mRNA expression by IL-1 and TNF suggests that the local pro-inflammatory action of these cytokines may be mediated by induction of chemotactic factor secretion. Volume 167 June 1988 1883-1893 Materials and Methods cDNA Cloning of MDNCF and Nucleotide Sequence . Normal human PBMC were first fractionated by Ficoll-Hypaque and plastic adherent cells (> 90% nonspecific esterase-positive monocytes), were cultured in RPMI-1640 medium supplemented with 1% FCS and 10 ug/ml LPS (Serotype 055:1155; Difco Laboratories Inc., Detroit, MI) for 6 h at 37°C . Total RNA

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The results indicate that proinflammatory type 1 genes regulated by IFN-gamma are similarly increased in both SP and LP psoriasis, but a potential difference in IL-18 exists between these disease forms. The consistent activation of this set of genes argues for a central role of IFN-gamma as a molecular regulator of inflammation in these distinct subtypes of psoriasis vulgaris. In contrast, disease extent/severity must be controlled by yet other factors.