Abstract: Disclosed is a novel polypeptide which can inhibit angiogenesis. Also disclosed is use of the polypeptide. The polypeptide comprises at least one amino acid sequence selected from the amino acid sequences depicted in SEQ ID NOs: 1-3, is composed of 120 or less amino acid residues, and has an anti-angiogenic activity. The polypeptide has an anti-angiogenic activity, has a lower molecular weight compared with that of PEDF, and has excellent penetration or absorption into a living body, particularly an affected part in a living body.

Abstract: Provided is a novel method for preventing or treating malignant melanoma, which comprises administering an effective amount of at least one selected from the group consisting of: a) a pigment epithelium-derived factor; b) a variant of the pigment epithelium-derived factor (a) that has the functionally equivalent properties to the factor (a); and c) a vector comprising such factor to a subject in need thereof.

Abstract: Disclosed are the identification of a differentiation pathway of cultured fibrocytes, characterization of the signals for fibrocyte migration to wound sites in vivo, and the potential role of fibrocytes in wound contracture. The invention relates to a method for producing fibrocytes comprising contacting a population of human peripheral blood mononuclear cells (PBMC) comprising predominantly CD14+ cells with autologous T cells or a form of TGF&bgr;, preferably TGF&bgr;1, thereby inducing differentiation of fibrocytes from precursors in the PBMC population. These fibrocytes are useful for treating a wound in a mammalian subject by administering fibrocytes to the subject, preferably in combination with TGF&bgr;1. Also disclosed are methods for attracting or targeting fibrocytes to a wound by administering SLC or another agonist of the CCR7 chemokine receptor, at or near the site of the wound, and methods of decreasing undesired wound fibrosis by inhibiting fibrocyte activity.

Abstract: Regulation of expression of CTL activity by macrophage migration inhibitory factor (MIF) is disclosed. In a mouse model using the EL4 tumor, cultured splenocytes from tumor-primed mice secrete high levels of MIF following antigen stimulation in vitro. Parallel splenocytes treated with neutralizing anti-MIF mAb showed a significant increase in CTL response against tumor cells compared to control mAb-treated cultures, with elevated expression of IFN&ggr;. Histology of tumors from anti-MIF treated animals showed increases in infiltration of both CD4+ and CD8+ T cells, as well as apoptotic tumor cells, consistent with observed augmentation of CTL activity in vivo by anti-MIF, which was associated with enhanced expression of the common &ggr;c chain of the IL-2 receptor that mediates CD8+T cell survival. CD8+ cells of anti-MIF treated tumor-bearing mice showed increased migration into tumors of control mice. Methods for enhancing a CTL response by inhibition of MIF are disclosed.