Disease relevance of POLY I-C

• Uptake of EA as enhanced by the extraperitoneal administration of Newcastle disease virus, vesicular stomatitis virus, tilorone or polyinosinic-polycytidylic acid [1].
• Uninfected monocytes also produced high levels of IFN-alpha after treatment with poly(I).poly(C), Newcastle disease virus, or herpes simplex virus [2].
• The kinetics and organ distribution patterns of lymph node natural killer (NK) cell activation or suppression were found to vary according to the type, dose, and route of administration of Corynebacterium parvum or polyinosinic-polycytidylic acid (poly I . poly C) [3].
• Combined immunostimulation with BCG and double-stranded polyinosinic-polycytidylic acid (poly I . poly C) was more effective than single-modality immunostimulation in suppressing tumor growth in inbred Swiss mice [4].
• Enhanced host resistance to transplantable murine lymphosarcoma in Swiss mice by combined immunostimulation with BCG and polyinosinic-polycytidylic acid [4].

Psychiatry related information on POLY I-C

• Administration of polyinosinic-polycytidylic acid, which activates NK activity but does not directly affect mammary epithelial cell growth, to HAN-bearing mice enhanced tumor progression, as measured by a decrease in the latency period and increase in the incidence of mammary adenocarcinomas developing in the HAN implants [5].

High impact information on POLY I-C

• Agents inducing NK-cell maturation or activation such as polyinosinic-polycytidylic acid (poly(I:C], interferon (IFN) and interleukin-2 (IL-2) restore NK activity, and normalize the number of LGL [6].
• However, both uninfected and HIV-infected monocytes produced high levels of each of these cytokines after treatment with synthetic double-stranded RNA [poly(I).poly(C)] [2].
• Although pretreatment with polyinosinic-polycytidylic acid enhanced in vitro NK cell activity, it could augment only slightly the clearance of YAC-1 cells from the lungs and the liver [7].
• The effect of polynucleotides poly(I).poly(C) and the complex of poly(I).poly(C) with poly-L-lysine and carboxymethylcellulose on HVS and EBV was also studied [8].
• Polyinosinic-polycytidylic acid: inhibition of cell proliferation in carcinogen-treated epidermis and in carcinogen-induced skin tumors in mice [9].

Chemical compound and disease context of POLY I-C

• Modulation of 5-fluorouracil-induced toxicity in mice with interferon or with the interferon inducer, polyinosinic-polycytidylic acid [10].
• Warfarin treatment increased the elimination of radiolabeled BL6 melanoma cells from the lungs of normal mice, and the rate of tumor cell elimination was further potentiated when NK cell activity was stimulated by polyinosinic-polycytidylic acid [11].
• Ameliorating effect of an interferon inducer polyinosinic-polycytidylic acid on bleomycin-induced lung fibrosis in hamsters. Morphologic and biochemical evidence [12].
• Activation of NK cells by polyinosinic-polycytidylic acid (poly I.C) and Corynebacterium parvum also was impaired in beta-estradiol-treated mice, whereas activation of tumoricidal macrophages was uncompromised [13].
• About 90% of T lymphoblast migration to IFN-gamma, IFN-gamma plus TNF-alpha, polyinosinic polycytidylic acid, lipopolysaccharide, and delayed-type hypersensitivity (DTH)-induced inflammation was inhibited [14].

Biological context of POLY I-C

• Murine cytomegalovirus (MCMV) infection and the TLR3 ligand polyinosinic-polycytidylic acid [poly(I:C)] were used to activate innate immunity [15].
• RESULTS: In the mouse model of DDC-induced liver fibrosis, natural killer cell activation by polyinosinic-polycytidylic acid induced cell death to activated hepatic stellate cells and attenuated the severity of liver fibrosis [16].
• Human beta-interferon gene expression is induced by virus or poly(I).poly(C) [17].
• This led to a blunted response to the hematopoietic stress induced by polyinosinic-polycytidylic acid, with a persistently low platelet count and hematocrit compared with controls [18].
• Virus or poly(I).poly(C) induction of human beta-interferon gene expression requires a 40-base-pair DNA sequence designated the interferon gene regulatory element (IRE) [19].

Anatomical context of POLY I-C

• Requirement for macrophages in in vitro augmentation, by interferon (IFN), polyinosinic-polycytidylic acid (poly I:C), or Corynebacterium parvum, of rat, mouse, and human natural killer (NK) activities was examined [20].
• Polyadenylylated mRNA was purified from poly(I).poly(C)- and cycloheximide-superinduced human fibroblast (FS-4) cultures [21].
• The oligoribonucleotide (2' goes to 5')(pA)3 also antagonizes the translational inhibitory capacity of poly(I).poly(C) in extracts of interferon-treated L cells, suggesting that (2' goes to 5')oligo(A) is the primary mediator of the protein synthesis inhibitory effects of poly(I).poly(C) in this cell-free system [22].
• Mast cells play an important role in host defense against various pathogens, but their role in viral infection has not been clarified in detail. dsRNA, synthesized by various types of viruses and mimicked by polyinosinic-polycytidylic acid (poly(I:C)) is recognized by Toll-like receptor 3 (TLR3) [23].
• In addition, these cell lines were killed in a 4-h NK cytotoxicity assay by polyinosinic-polycytidylic acid-activated effector lymphocytes [24].

Associations of POLY I-C with other chemical compounds

• Human tumor necrosis factor alpha (TNF-alpha) gene expression can be induced primarily in cells of the monocyte/macrophage lineage by a variety of inducers, including lipopolysaccharide, phorbol esters such as phorbol 12-myristate 13-acetate, and virus or synthetic double-stranded RNA [poly(I).poly(C)] [25].
• Like dopamine, morphine'e effect on the adenylate cyclase activity was increased or decreased, respectively, by pretreating the animals with poly(I).poly(C) or with chloramphenicol [26].
• Inhibition of cancer cell growth by polyinosinic-polycytidylic acid/cationic liposome complex: a new biological activity [27].
• Antagonistic effect of polyinosinic-polycytidylic acid on the cell lethality produced by 5-fluorouracil in human colon carcinoma cells in vitro [28].
• When mice were treated with anticoagulants (warfarin or heparin) or when NK cell activity was stimulated by polyinosinic-polycytidylic acid, significant antimetastatic effects were observed; these effects were substantially augmented when the treatments were combined [11].

Gene context of POLY I-C

• Poly(rI).poly(rC) appeared to be a better inducer for M-CSF than IL-1 [29].
• Polyinosinic-polycytidylic acid (poly I:C) or IFN-gamma treatment inhibited liver fibrosis in wild-type mice but not in STAT1(-/-) mice [30].
• PCT-GF activity in supernatants of human FS-4 fibroblasts stimulated with TNF, IL-1 or poly(I).poly(C) was neutralized by antibody to rBSF-2, but not by antibodies neutralizing the antiviral activity of IFN-beta [31].
• Treatment with polyinosinic-polycytidylic acid to induce expression of Cre resulted in complete disruption of the Arnt gene and loss of ARNT messenger RNA (mRNA) expression in liver [32].
• RESULTS: Serum samples positive for NAbs significantly inhibited polyinosinic-polycytidylic acid-induced CXCL10 and IL-6 production by astrocytes [33].

Analytical, diagnostic and therapeutic context of POLY I-C

• Pre-VAF and VAF rats have essentially the same lymphocyte subsets, and VAF-DP rats are susceptible to the adoptive transfer of diabetes and to the diabetes-accelerating effects of polyinosinic-polycytidylic acid injections [34].
• Northern blot analysis reveals that total RNA from human fibroblastoid cells (MG 63) induced with poly(I).poly(C) under conditions of IFN-beta production, contains predominantly a +/- 1,200 nucleotide long poly (A) mRNA (mRNA.M) which hybridizes with a Hu IFN-beta cDNA specific probe [35].
• Scatchard plots of the binding of [(terpy)Pt(HET)]+ to poly(A).poly(U) and poly(I).poly(C), determined through ultracentrifugation pelleting methods, show large positive curvature, reflecting the strong cooperativity associated with the platinum complex-RNA interaction [36].
• Blood LGL cultured in cell impermeable diffusion chambers in the peritoneal cavity of poly(I).poly(C)-stimulated rats exhibited enhanced natural killer (NK) activity but no proliferative response, indicating that mature LGL were not induced to undergo blastogenesis by poly(I).poly(C) in vivo [37].
• Indirect immunofluorescence revealed that 13% of BALB/c and 33% of CBA spleen cells of B type carry specific binding sites at their surface for double-stranded poly(I).poly(C) [38].

References