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  • 1
    Keywords: PEPTIDE ; CELLS ; BLOOD ; CELL ; Germany ; human ; VIVO ; PROTEIN ; PROTEINS ; MICE ; RESPONSES ; INFECTION ; FAMILY ; DONOR ; T cells ; T-CELLS ; MEMBER ; MEMBERS ; MEMORY ; TRANSGENIC MICE ; IDENTIFICATION ; CELL-LINE ; LINE ; LYMPHOCYTES ; PEPTIDES ; EPITOPE ; HUMAN DENDRITIC CELLS ; FAMILIES ; ESCAPE ; VIRULENCE ; T helper cells ; BACTERIA ; spleen ; immune responses ; bacterial infection ; GROUP-A STREPTOCOCCUS ; LISTERIA-MONOCYTOGENES ; PNEUMOLYSIN
    Abstract: Cholesterol-binding cytolysins constitute an evolutionarily conserved family of pore-forming proteins expressed by different Gram-positive pathogens. Listeriolysin O, one well-characterized member of the cytolysin family, is also known to induce specific CD4 and CD8 T cell responses upon infection of mice with Listeria monocytogenes. Here we describe an HLA-DRB1*0301-restricted listeriolysin O-derived T cell epitope that is conserved among several members of the cytolysin family. An HLA-DRB1*0301-restricted CD4+T cell line, established from spleen lymphocytes of L. monocytogenes-infected HLA-DRB1*0301-transgenic mice, cross-reacted with a homologous peptide from perfringolysin O, a cytolysin expressed by Clostridium peifringens. Ex vivo analysis of infected mice revealed an even broader cross-reaction of T cells with homologous peptides derived from perfringolysin O, streptolysin O, and cereolysin O. Interestingly, a cross-reactive memory CD4+T cell response against the homologous peptides derived from listeriolysin O and perfringolysin O could also be detected in the blood from healthy HLA-DRB1*0301(+) human donors. Remarkably, this response was even present in donors who did not exhibit a memory T cell reactivity against a second, non-conserved HLA-DRB1*0301-restricted LLO-derived CD4 T cell epitope, suggesting that cytolysin-producing bacteria other than L. monocytogenes can stimulate a cross-reactive cytolysin-specific immunity. (c) 2006 Elsevier SAS. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16798043
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  • 2
    Keywords: proliferation ; DENDRITIC CELLS ; T-CELLS ; IDENTIFICATION ; SIGNALING PATHWAYS ; IMMUNITY ; TARGETS ; p38 MAPK ; EXPERIMENTAL AFRICAN TRYPANOSOMIASIS ; MACROPHAGE ACTIVATION
    Abstract: To identify miRNAs whose expression are differentially regulated during trypanosome infections a microarray targeting more than 600 rat miRNA was used to analyze the miRNA expression profiles between uninfected rats and animals infected by Trypanosoma congolense and Trypanosoma brucei s.l. The potential targets of dysregulated miRNAs as well as their biological pathways and functions were predicted using several bioinformatics software tools. Irrespective of the infecting trypanosome species, eight miRNAs (seven up- and one down-regulated) were dysregulated during infections. Moreover, other miRNAs were differentially regulated in rats infected by specific trypanosome species. Functional analyses of differentially regulated miRNAs indicated their involvement in diverse biological processes. Among these, transcription repressor activity, gene expression control as well as protein transporter activity were predominant. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis of dysregulated miRNAs revealed their involvement in several biological pathways and disease conditions. This suggests possible modulation of such pathways following trypanosome infection; for example, the MAPK signaling pathway which is known to play vital roles in apoptosis, innate immune response and response to viral infections was highly affected. Axon guidance was equally highly impacted and may indicate a cross reactivity between pathogen proteins and guidance molecules representing one pathological mechanism as it has been observed with influenza HA. Furthermore, Ingenuity pathway analyses of dysregulated miRNAs and potential targets indicated strong association with inflammatory responses, cell death and survival as well as infectious diseases. The data generated here provide valuable information to understand the regulatory function of miRNAs during trypanosome infections. They improved our knowledge on host-parasite cross-talks and provide a framework for investigations to understand the development of trypanosomes in their hosts as well as the differences in the clinical and pathological evolutions of the disease.
    Type of Publication: Journal article published
    PubMed ID: 25797398
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  • 3
    Keywords: CANCER ; EXPRESSION ; tumor ; Germany ; IN-VIVO ; THERAPY ; VIVO ; SYSTEMS ; GENE ; GENE-EXPRESSION ; MOLECULES ; TISSUE ; MICE ; INDUCTION ; gene expression ; ESCHERICHIA-COLI ; VECTOR ; PROMOTER ; NETHERLANDS ; BIOLUMINESCENCE ; ENGINEERED BACTERIA ; Gall bladder ; In vivo imaging ; Inducible promoter ; Organ colonization ; Tumor targeted bacteria
    Abstract: The probiotic bacterium Escherichia coli Nissle 1917 (EcN) constitutes a prospective vector for delivering heterologous therapeutic molecules to treat several human disorders. To add versatility to this carrier system, bacteria should be equipped with expression modules that can be regulated deliberately in a temporal and quantitative manner. This approach is called in vivo remote control (IVRC) of bacterial vectors. Here, we have evaluated promoters P-araBAD, P-rhaBAD and P-tet, which can be induced with L-arabinose, L-rhamnose or anhydrotetracycline, respectively. EcN harboring promoter constructs with luciferase as reporter gene were administered either orally to healthy mice or intravenously to tumor bearing animals. Subsequent to bacterial colonization of tissues, inducer substances were administered via the oral or systemic route. By use of in vivo bioluminescence imaging, the time course of reporter gene expression was analyzed. Each promoter displayed a specific ill vivo induction profile depending on the niche of bacterial residence and the route of inducer administration. Importantly, we also observed colonization of gall bladders of mice when EcN was administered systemically at high doses. Bacteria in this anatomical compartment remained accessible to remote control of bacterial gene expression.
    Type of Publication: Journal article published
    PubMed ID: 19665575
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  • 4
    Keywords: Germany ; GENE-EXPRESSION ; PROTEIN ; PROTEINS ; RNA ; transcription ; COMPLEX ; COMPLEXES ; DYNAMICS ; BIOLOGY ; TRANSCRIPTIONAL ACTIVITY ; acetylation ; HISTONE ACETYLTRANSFERASE ; PCAF BROMODOMAIN ; POSTTRANSLATIONAL MODIFICATIONS ; IMMUNODEFICIENCY-VIRUS TYPE-1 ; RNA-POLYMERASE-II ; review ; REVERSE TRANSCRIPTION ; interaction ; HIV ; Tat ; TAT PROTEIN ; posttranslational modification ; P-TEFB
    Abstract: The Tat protein is a viral transactivator that activates HIV transcription through complex interactions with RNA and host cell factors. Tat undergoes multiple posttranslational modifications that regulate the dynamics and complexity of these interactions. The biology of these modifications and their role in Tat function are reviewed. (c) 2005 Elsevier SAS. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16046164
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