In this paper, we report the synthesis of several anthrylazamacrocycles designed to provide chelation-enhanced fluorescence on complexation of nonquenching metal ions [e.g., Zn(II) and Cd(II)] in totally aqueous solution. The N3, N4, N5, and N6 derivatives are water-soluble compounds whose fluorescence is enhanced by addition of Zn(II) and Cd(II) and

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Several groups have reported observing fluorescence enhancements in nonaqueous solutions upon the binding of some metal ions to conjugate fluorescent probes, probes in which the metal ligand is not an integral part of the fluorophorc substructure.2 Conjugate probes offer great potential as reporter molecules in that the known selectivities of azacrown and cryptand binding sites can, in principle, be applied unaltered to the design of fluorescent probes with similar selectivities and large signal ranges. Recently, we have found that anthrylazamacrocycles demonstrate

SummaryInterferon (IFN) ",/, a cardinal proinflammatory cytokine, induces expression of the gene products of the class II locus of the major histocompatibility complex (MHC), whereas IFN-0t or -[3 suppresses MHC class II expression. The mechanism of IFN-13-mediated MHC class II inhibition has been unclear. Recently, a novel factor termed class II transactivator (CIITA) has been identified as essential for IFN-~/-induced MHC class II transcription. We studied the status of IFN-~/-induced CIITA messenger P, NA (mI(NA) accumulation and CIITA-driven transactivation in IFN-13-treated cells and used cell lines that had defined defects in the type I IFN response pathway to address the roles of IFN signaling components in the inhibition of MHC class II induction. IFN-~ treatment did not suppress IFN-~-induced accumulation of CIITA mR~A. After cells were stably transfected with CIITA, endogenous MHC class II genes were constitutively expressed, and MHC class II promoters, delivered by transfection, were actively transcribed in CIITA-expressing cells. Expression of these promoters was significantly impaired by pretreatment with IFN-[3. These results suggest that IFN-[3 acts downstream of CIITA mRNA accumulation, and acts in part by reducing the functional competence of CIITA for transactivating MHC class II promoters. IFN stimulated gene factor 3 (ISGF3) was essential for IFN-[3 to mediate inhibition of MHC class II induction, regardless of whether MHC class II transcription was stimulated by IFN-~ or directly by CIITA expression. Results of these experiments suggest that inhibition of MHC class II in IFN-[3-treated cells requires expression of gene(s) directed by the ISGF3-IFN-stimulated response element pathway, and that these gene product(s) may act by blocking CIITA-driven transcription of MHC class II promoters.

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