Disease relevance of Cxcl11

• A recombinant vaccinia virus encoding the interferon-inducible T-cell alpha chemoattractant is attenuated in vivo [1].
• In the lungs from mice infected with RSV or influenza A viruses, peak expression of I-TAC coincided with peak viraemia [1].
• IP-10, Mig, and IP-9 mRNA were detected in seven of nine allergic contact dermatitis reactions after 24-72 h, but not in sodium lauryl sulfate-induced irritant contact dermatitis reactions [2].
• To investigate this, mice were challenged with EL4 T-cell lymphoma cells, genetically modified to produce murine CXCL11 [3].
• Blepharitis and clinical signs of infection were evident in IFN-alpha/betaR-/- and IFN-alpha/beta/gammaR-/- but not control mice for all viruses [4].

Psychiatry related information on Cxcl11

• Moreover, food deprivation led to a greater increase in hypothalamic mOX2 beta R gene expression, compared with both mOX1R and mOX2 alpha R. This potentially implicates a fundamental physiological role for these splice variants [5].

High impact information on Cxcl11

• In this study, we addressed the role of type I IFNs by examining the infection of L. monocytogenes in BALB/c mice lacking the type I IFN receptor (IFN-alpha/betaR-/-) [6].
• Resistance was correlated with elevated levels of interleukin 12p70 in the blood and increased numbers of CD11b+ macrophages producing tumor necrosis factor alpha in the spleen of IFN-alpha/betaR-/- mice [6].
• In addition, the intracellular fate of L. monocytogenes in macrophages cultured from IFN-alpha/betaR-/- and wild-type mice was indistinguishable [6].
• Particularly striking was restoration of near-normal trigeminal ganglion replication and neurovirulence of an ICP34.5 mutant in IFN-alpha/betaR-/- mice [4].
• Anti-LT-beta-R mAbs were also identified that inhibited ligand-induced cell death, whereas others were found to potentiate the activity of the ligand when added in solution [7].

Biological context of Cxcl11

• Taken together, these studies suggest that IP-10, MIG, I-TAC, and CXCR3 interactions are involved in mucosal immune responses required for the induction of CD [8].
• Monokine-induced by IFN-gamma (MIG), IFN-gamma-inducible T cell alpha chemoattractant (I-TAC), and IFN-gamma-inducible protein-10 (IP-10), are chemokines that bind CXCR3 and mediate the chemotaxis of leukocytes [8].
• The nucleotide sequence of Scyb11 shares 63% identity with its human counterpart [9].
• Using a BAC clone containing Scyb11, this gene could be mapped to chromosome 5 at position 5E3 [9].
• A genomic sequence was obtained by genome walking and subcloning DNA fragments from a BAC clone containing Scyb11 [9].

Anatomical context of Cxcl11

• To better understand the role of CXCR3 interactions during CD, we characterized the effects of IP-10, MIG, I-TAC, and CXCR3+ T cells on mucosal immune responses [8].
• Pretreatment with dexamethasone strongly attenuates both IFN-gamma-induced I-TAC expression in RAW cells and endotoxemia-induced I-TAC expression in lung and small intestine [10].
• RNA transcripts encoding PDGF-B and PDGF-beta R are expressed by cells of the hyaloid and mature vascular systems in the eye and optic nerve [11].
• IFN-alpha/betaR(-/-) mice cleared low-dose intranasal gammaHV68 infection with wt kinetics and harbored essentially wt frequencies of latently infected cells in both peritoneum and spleen by 28 days postinfection [12].
• IFN-alpha/betaR-/- mice also demonstrated altered cellular tropism, with increased infection in macrophages, B cells, and T cells in the spleen [13].

Associations of Cxcl11 with chemical compounds

• Here, we cloned the cDNA of the murine homologue of this protein, Scyb11, from interferon-gamma/lipopolysaccharide-stimulated RAW264.7 mouse macrophage-like cells [9].
• Intron 1 of Scyb11 is also characterized by a 201-bp stretch with repetitive sequences of high cryptic simplicity [9].
• The action of core 2 GlcNAc-transferase followed by beta 1-4Gal-transferase provides an N-acetyllactosamine antenna that can be extended with polylactosamine (i.e. repeating Gal beta 1-4GlcNAc beta 1-3) provided UDP-GlcNAc:Gal beta-R beta 1-3GlcNAc-transferase (GlcNAc-transferase) (i)) activity is present [14].
• The angiogenic activity in the lung was significantly decreased, however, and CXCL11 treatment reduced the total number of endothelial cells in the lung following bleomycin exposure [15].
• However, a single administration of CORT to adrenalectomized mice significantly decreased the mRNA levels of IFN-alpha/beta R1 in the liver [16].

Regulatory relationships of Cxcl11

• IFN-gamma regulates murine interferon-inducible T cell alpha chemokine (I-TAC) expression in dendritic cell lines and during experimental autoimmune encephalomyelitis (EAE) [17].

Other interactions of Cxcl11

• 2. Recently, we identified mouse Scyb11 and mapped this gene by fluorescence in situ hybridization (FISH) to mouse Chr 5E3, the orthologous locus to human 4q21 where the other two homologous mouse genes, Scyb9 and Scyb10, have also been localized [18].
• In vivo trafficking assays demonstrated a requirement for IFN-alpha/betaR signaling for leukocyte localization in, and delivery of MIP-1alpha-producing macrophages to, the liver [19].
• To identify novel mechanisms involved in combating intracellular infections, experiments were performed in mice with selective defects in the lymphotoxin (LT)/LT beta R pathway [20].
• IRF-7 and IRF-9 gene expression was increased in LCMV-infected brain from IFN-gamma knockout (KO) but not IFN-alpha/betaR KO animals [21].
• Overnight treatment of 32D/PDGF-beta R/PKC-delta cells with PDGF-BB induced monocytic differentiation as judged by an increase in expression of cell surface macrophage differentiation markers [22].

Analytical, diagnostic and therapeutic context of Cxcl11

• We analysed I-TAC expression by reverse transcriptase-polymerase chain reaction during three different virus-infection models in mice, respiratory syncytial virus (RSV), influenza A and vaccinia virus western reserve (VV-WR) [1].
• These experiments show, for the first time, antitumor activity of CXCL11 in vivo, which warrants exploration for its potential role in anticancer immunotherapy [3].
• Tumor infiltrate analysis by flow cytometry showed a clear correlation between rejection of CXCL11-producing tumors and an increase of tumor-infiltrating CD8+CXCR3+ as well as CD8+CXCR3- T lymphocytes [3].
• However, in IFN-alpha/betaR-/- or IFN-alpha/beta/gammaR-/- mice, growth of all mutants, including those with significantly impaired growth in cell culture, was enhanced by up to 1,000-fold in eyes and trigeminal ganglia [4].
• PCR analysis of beta M beta R double transgenic mice revealed almost complete suppression of endogenous TCR V beta gene rearrangements, but blockage of minilocus V beta rearrangements was achieved with only one of five minilocus transgenic lines [23].

References