@article{BotheAguzziLassmannetal.1991, author = {Bothe, Katrin and Aguzzi, Adriano and Lassmann, Hans and Rethwilm, Axel and Horak, Ivan}, title = {Progressive encephalopathy and myopathy in transgenic mice expressing human foamy virus genes}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61453}, year = {1991}, abstract = {Transgenie mice carrying the bel region of human foamy retrovirus (HFV) under transcriptional control of its own long terminal repeat expressed tbe transgene in their centrat nervous systems and in smootb and striated muscle tissues. The animals developed a progressive degenerative disease of tbe centrat nervous system and of the striated muscle. Because expression of tbe transgene was dosely correlated witb the appearance of structural damage and inflammatory reactions were scanty, the disease is likely to be caused directly by tbe HFV proteins. These unexpected findings call for a reevaluation of tbe patbogenic potential of HFV in humans.}, subject = {Virologie}, language = {en} } @article{MaurerSerflingterMeulenetal.1991, author = {Maurer, Bernd and Serfling, Edgar and ter Meulen, Volker and Rethwilm, Axel}, title = {Transcription factor AP-1 modulates the activity of the human foamy virus long terminal repeat}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61444}, year = {1991}, abstract = {The human foamy virus (HFV) contains within the UJ region of its long terminal repeat (L TR) three perfect consensus sequences for the binding of the inducible transcription factor AP-1. Results of DNase I footprint protection and gel retardation assays demonstrated that proteins in extracts of HeLa and BHK-21 cells as weil as bacterially expressed Jun and Fos proteins bind to these AP-1 sites. By conducting transient expression assays using chloramphenicol acetyltransferase plasmids carrying LTR sequences with point-mutated AP-1 sites it was found that the three AP-1 sites contribute to the optimal activity ofthe HFV promoter. It is shown that lnduction of the HFV L TR by 12-O-tetradecanoylphorbol-13-acetate (TPA) and serum factors is mediated through the AP-1 sites.}, subject = {Virologie}, language = {en} } @article{GowSimpsonSchliephakeetal.1992, author = {Gow, J. W. and Simpson, K. and Schliephake, Andreas and Behan, W. M. and Morrison, L. J. and Cavanagh, H. and Rethwilm, Axel and Behan, P. O.}, title = {Search for retrovirus in the chronic fatigue syndrome}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61436}, year = {1992}, abstract = {Aim: To examine peripheral blood and skeletal muscle from patients with chronic fadgue syndrome for exogenous retrovirus. Methods: Blood samples from 30 patients and muscle biopsy specimens of 15 patients were examined for retroviral sequences by DNA extraction, polymerase chain reacdon (PCR), and Southern blotting hybridisation. Sera were examined for human foamy virus by western immunoblotting and indirect immunofluorescence techniques. Results: No difference between the padent and control populations was found for any of the PCR primer sets used (gag, pol, env, and tax regions of HTLV VII). An endogenous gag band was observed in both the padent and control groups. All sera were negative for antibody to human foamy virus. Conclusion: The results indicate that there is no evidence of retroviral involvement in the chronic fatigue syndrome.}, subject = {Virologie}, language = {en} } @article{NetzerSchliephakeMaureretal.1993, author = {Netzer, Kai O. and Schliephake, Andreas and Maurer, Bernd and Watanabe, Rihito and Aguzzi, Adriano and Rethwilm, Axel}, title = {Identification of pol-related gene products of human foamy virus}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61429}, year = {1993}, abstract = {Human foamy viruspol gene fragments were molecularly cloned into a procaryotic expression vector. The expression pattern of the cloned fragments and nucleotide sequence analysis of the 5' pol gene region revealed that in HFV the protease (PR) is located in the pol open reading frame. Purified recombinant proteins were used to generate antibodies in rats. ln immunoblot assay, using infected cells as antigen, a precursor protein with an apparent molecular mass (M,) of 127K was identified by antibodies directed against the reverse transcriptase (RT), RNaseH, or integrase (IN) domeins of pol. With concentrated virus as antigen, the RT and RNaseH antibodies recognized a protein of 80K, the IN antiserum recognized a protein of 40K, and the PR antiserum detected a protein of approximately 10K.}, subject = {Virologie}, language = {en} } @article{BrinkmannSchwinnMuelleretal.1993, author = {Brinkmann, R. and Schwinn, A. and M{\"u}ller, J. and Stahl-Hennig, C. and Coulibaly, C. and Hunsmann, G. and Czub, S. and Rethwilm, Axel and D{\"o}rries, R. and ter Meulen, Volker}, title = {In vitro and in vivo infection of rhesus monkey microglial cells by simian immunodeficiency virus}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61415}, year = {1993}, abstract = {The observation that microglial cells in brain tissue are probably a major target for human immunodeficiency virus (HIV) infection has raised interest in the pathogenic role of this cell population for the development of neuro-AIOS. Since it is very difficult to obtain microglia from normal or diseased human brain we studied microglial cells isolated from fresh brain tissue of uninfected and simian immunodeficiency virus (SIV) infected rhesus monkeys (Macacca mulatta) in comparison to peripheral blood macrophages. Besides the characterization of the phenotypes of these two cell populations, we examined the replication of SIV in the cells in addition to the effect of viral infection on the expression of cell surface molecules. We found that microglia and macrophages support replication of the wild-type SIV\(_{mac25}\), strain as well as the infectious clone (SIV\(_239\)). Infectious viruswas produced and a CPE developed. Isolated microglial cells from SIV-infected monkeys were latently infected independent of the presence of neuropathological lesions and produced infectious virus after 20-25 days in culture. In situ hybridization revealed that only a small percentage of isolated microglial cells are productively infected in vivo, yet the majority of these expressed MHC class II molecules. This indicated a state of activation that is acquired in vivo. These findings indicate that microglia are a prime target cell for SIV infection in CNS tissue.}, subject = {Virologie}, language = {en} } @article{ErlweinRethwilm1993, author = {Erlwein, Otto and Rethwilm, Axel}, title = {BEL-1 transactivator responsive sequences in the long terminal repeat of human foamy virus}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61402}, year = {1993}, abstract = {No abstract available}, subject = {Virologie}, language = {en} } @article{BaunachMaurerHahnetal.1993, author = {Baunach, Gerald and Maurer, Bernd and Hahn, Heidi and Kranz, Manuela and Rethwilm, Axel}, title = {Functional analysis of human foamy virus accessory reading frames}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61398}, year = {1993}, abstract = {No abstract available}, subject = {Virologie}, language = {en} } @article{HongBraeutigamRethwilm1993, author = {Hong, Liu and Br{\"a}utigam, Sandra and Rethwilm, Axel}, title = {Expression of the human foamy virus bel-1 transactivator in insect cells}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61383}, year = {1993}, abstract = {The human foamy virus (HFV) bel-l transactivator protein was expressed in insect cells by a recombinant baculovirus. For the generation of the recombinant baculovirus, Acbel-1, the bel-l gene of an HFV mutant was used, that bears truncations in the bel-l overlapping bel-2 open reading frame. Acbel-1 infected Sf9 cells produced high amounts of recombinant protein of the same electrophoretic mobility (36 kD) as bel-l expressed in mammalian cells. The baculovirus expressed bel-l proteinwas readily identified by a polyclonal rabbit serum directed against bel-1 in immunoblot assay. As in mammalian cells, bel-l was predominantly localized to the nucleus of Acbel-1 infected insect cells. The baculovirus expressed bel-1 proteinwill be of use to determine the action of this novel viral transactivator more precisely.}, subject = {Virologie}, language = {en} } @article{SchliephakeRethwilm1994, author = {Schliephake, Andreas W. and Rethwilm, Axel}, title = {Nuclear Localization of Foamy Virus Gag Precursor Protein}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61371}, year = {1994}, abstract = {All foamy viruses give rise to a strong nuclear staining when infected cells are reacted with sera from infected hosts. This nuclear ftuorescence distinguishes foamy viruses from all other retroviruses. The experiments reported here indicate that the foamy virus Gag precursor protein is transiently located in the nuclei of infected cells and this is the likely reason for the typical foamy virus nuclear fluorescence. By using the vaccinia virus expression system, a conserved basic sequence motif in the nucleocapsid domain of foamy virus Cag proteins was identified to be responsible for the nuclear transport of the gag precursor molecule. Tbis motif was also found to be able to direct a heterologous protein, the Gag protein of human immunodeficiency virus, into the nucleus.}, subject = {Virologie}, language = {en} } @article{HahnBaunachBraeutigametal.1994, author = {Hahn, Heidi and Baunach, Gerald and Br{\"a}utigam, Sandra and Mergia, Ayalew and Neumann-Haefelin, Dieter and Daniel, Muthiah D. and McClure, Myra O. and Rethwilm, Axel}, title = {Reactivity of primate sera to foamy virus Gag and Bet proteins}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61366}, year = {1994}, abstract = {In order to establish criteria for the Serodiagnosis of foamy virus infections we investigated the extent to which sera from iofected individuals of human and primate origin react with structural and non-structural virus proteins in immunoblot assays. Using lysates from infected cells as the source of virus antigen, antibodies were preferentially detected against the Gag proteins and the non-structural Bet protein. Both the Gag precursor molecules of 70 and 74K apparent M\(_r\) and the cytoplasmic 60K M\(_r\) Bet protein were found to be phosphorylated, the latter being synthesized in large amounts in infected cells. Rahbit antiserum raised against recombinant human foamy virus (HFV) Gag major capsid protein cross-reacted with foamy viruses of chimpanzee, gorilla, orang-utan, rhesus monkey and Mrican green monkey origin. This was reßected by a broad cross-reactivity of the respective monkey sera to the Gag proteins of the various foamy virus isolates. Cross-reactivity of antisera against the Bet protein was restricted to viruses from man and the great apes. Recombinant Gag and Bet proteins expressed in prokaryotes or in insect cells were readily recognized by foamy virus-positive primate sera. Screening serum samples from chimpanzees with HFV Gag and Bet proteins expressed by recombinant baculoviruses revealed that 18 out of 35 (52\%) were positive for Gag antibodies. Of these, 13 (72 o/o) showed antiborlies against the Bet protein, indicating that Bet antigen is of value in sero1ogical screening for foamy virus infections.}, subject = {Virologie}, language = {en} } @article{SiwkaSchwinnBaczkoetal.1994, author = {Siwka, Wieslaw and Schwinn, Andreas and Baczko, Knut and Pardowitz, Iancu and Mhalu, Fred and Shao, John and Rethwilm, Axel and ter Meulen, Volker}, title = {vpu and env sequence variability of HIV-1 isolates from Tanzania}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61355}, year = {1994}, abstract = {No abstract available}, subject = {Virologie}, language = {en} } @article{KerkauGernertKneitzetal.1992, author = {Kerkau, T. and Gernert, S. and Kneitz, C. and Schimpl, A.}, title = {Mechanism of MHC class I downregulation in HIV infected cells}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-56849}, year = {1992}, abstract = {HIV infection of CD4+ peripheral blood lymphocytes leads to a loss of MHC dass I molecules on the surface of the infected cells as detectable by monodonal antibody staining and flow cytometry. Incubation of the infected cells at 26 oe or treatment at 37 oe with peptides leads to upregulation of MHC dass I to levels equal to those found on uninfected cells cultured und er the same conditions. The data suggest that, after HIV infection, the mechanisms responsible for peptide generation, peptide transport and thus stable association between peptides and MHC dass I molecules are severely affected.}, subject = {HIV}, language = {en} } @article{AguzziBothAnhauseretal.1992, author = {Aguzzi, A. and Both, K. and Anhauser, I. and Horak, I. and Rethwilm, Axel and Wagner, EF.}, title = {Expression of human foamy virus is differentially regulated during development in transgenic mice}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-55290}, year = {1992}, abstract = {Tbe human foamy virus (HFV) is a recently characterized member ofthe spumavirus family. Although no diseases have been unequivocally associated with HFV infection, expression of HFV regulatory genes in transgenie mice induces a characteristic aeute neuro degenerative disease and a myopathy. To better eharaeterize the sequenee of events leading to disease, and to gain a better understanding of the underlying pathogenetic meehanisms, we have analyzed in detail the transgene expression pattern during development. Transcription of a construet containing all regulatory elements and aneillary genes of mv was analyzed by in situ hybridization and was shown to occur in two distinct phases. At midgestation, low but widespread expression was first deteeted in eells of extraembryonie tissues. Later, various tissues originating from embryonie mesoderm, neuroeetoderm, and neural erest transeribed the transgene at moderate levels. However, expression deereased dramatically during late gestation and was suppressed shortly after birth. After a latency period of up to 5 weeks, transeription of the transgene resumed in single eelJs distributed irregularly in the central nervous system and in the skeletal museIe. By the age of 8 weeks, an increasing number of eells displayed much higher expression levels than in embryonie Iife and eventually underwent severe degenerative ehanges. These findings demonstrate that HFV transgene expression is differentially regulated in development and that HFV cytotoxicity may be dose-dependent. Such biphasic pattern of expression differs from that of murine retroviruses and may be explained by the specificity of HFV regulatory elements in combination with cellular faetors. Future studies of this model system should, therefore, provide novel insights in the mechanisms controlling retrovirallatency.}, subject = {Virologie}, language = {en} } @article{SchneiderSchauliesKirchhoffArchelosetal.1991, author = {Schneider-Schaulies, J{\"u}rgen and Kirchhoff, F. and Archelos, J. and Schachner, M.}, title = {Downregulation of Myelin Associated Glycoprotein (MAG) on Schwann cells by interferon-gamma and tumor necrosis factor-alpha affects neurite outgrowth}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54850}, year = {1991}, abstract = {To investigate the influence of inflammatory cytokines on the potential of peripheral nerves to regenerate, we analyzed the effect of interferon-y (lFN-y) and tumor necrosis factor-a (TNF-a) on the ability of immortalized Schwann cells to mediate outgrowth of neurites from primary DRG neurons. We found that IFN-y and TNF-a synergistically inhibited the neurite outgrowth-promoting properties of the Schwann cells by spedfically dowllregulating myelin-associated glycoprotein (MAG) at the levels of mRNA and cell surface protein by approximately 60\%. Antibodies to MAG inhibited the outgrowth of neurites on Schwann cells to the same extent as treatment with the two cytokines. Since MAG appears to be involved in both neurite outgrowth and myelination, our findings may provide evidence for a mechanism, by wh ich inflammatory cytokines interfere with Schwann cell-neuron interactions.}, subject = {Immunologie}, language = {en} } @article{SchneiderSchauliesKnauerHuenigetal.1984, author = {Schneider-Schaulies, J{\"u}rgen and Knauer, R. and H{\"u}nig, T. and Schimpl, A. and Wecker, E.}, title = {Induction of c-onc expression in polyclonally activated mouse lymphocytes}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54784}, year = {1984}, abstract = {No abstract available}, subject = {Lymphozyt}, language = {en} } @article{GrummtWeinmannDorschSchneiderSchauliesetal.1986, author = {Grummt, F. and Weinmann-Dorsch, C. and Schneider-Schaulies, J{\"u}rgen and Lux, A.}, title = {Zinc as a second messenger of mitogenic induction}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54799}, year = {1986}, abstract = {DNA synthesis and adenosine(S')tetraphosphate(S ')adenosine (Ap.A) levels decrease in cells treated with EDTA. The inhibitory effect of EDTA can be reversed with micro molar amounts of ZnCI2• ZnCh in micromolar concentrations also inhibits Ap.A hydrolase and stimulates amino acid-dependent Ap.A synthesis, suggesting that Zn2+ is modulating intracellular Ap.A pools. Serum addition to GI-arrested cells enhances uptake of Zn, whereas serum depletion leads to a fivefold decrease of the rates of zinc uptake. These results are discussed by regarding Zn2+ as a putative 'second messenger' of mitogenic induction and Ap.A as a possible 'third messenger' and trigger of DNA synthesis.}, subject = {Immunologie}, language = {en} } @article{SchneiderSchauliesKnauerSchimpletal.1987, author = {Schneider-Schaulies, J{\"u}rgen and Knauer, R. and Schimpl, A. and Wecker, E.}, title = {Cellular Oncogenes and lymphocyte activation}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54836}, year = {1987}, abstract = {No abstract available}, subject = {Lymphozyt}, language = {en} } @article{ArchelosRoggenbuckSchneiderSchauliesetal.1993, author = {Archelos, JJ and Roggenbuck, K. and Schneider-Schaulies, J{\"u}rgen and Linington, C. and Toyka, KV and Hartung, H.-P.}, title = {Production and characterization of monoclonal antibodies to the extracellular domain of PO}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54889}, year = {1993}, abstract = {Seven monoclonal antibodies were raised against the immunoglobulin-like extracellular domain of PO (POED), the major protein of peripheral nervous system myelin. Mice were immunized with purified recombinant rat PO-ED. After fusion, 7 clones (POI-P07) recognizing either recombinant, rat, mouse, or human PO-ED were selected by ELlS A and were characterized by Western blot, immunohistochemistry, and a competition assay. Antibodies belonged to the IgG or IgM class, and P04-P07, reacted with PO in fresh-frozen and paraffin-embedded sections of human or rat peripheral nerve, but not with myelin proteins of the central nervous system of either species. Epitope specificity of the antibodies was determined by a competition enzyme-linked immunosorbent assay (ELISA) and a direct ELlS A using short synthetic peptides spanning the entire extracellular domain of PO. These assays showed that POl and P02 exhibiting the same reaction pattern in Western blot and immunohistochemistry reacted with different distant epitopes of PO. Furthermore, the monoclonal antibodies P05 and P06 recognized 2 different epitopes in close proximity within the neuritogenic extracellular sequence of PO. This panel of monoclonal antibodies, each binding to a different epitope of the extracellular domain of PO, will be useful for in vitro and in vivo studies designed to explore the role of PO during myelination and in demyelinating diseases of the peripheral nervous system.}, subject = {Immunologie}, language = {en} } @article{AguzziWagnerNetzeretal.1993, author = {Aguzzi, A. and Wagner, E. F. and Netzer, K. O. and Bothe, K. and Anhauser, I. and Rethwilm, Axel}, title = {Human foamy virus proteins accumulate in neurons and induce multinucleated giant cells in the brain of transgenic mice}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47356}, year = {1993}, abstract = {Humanfoamy virus (HFV) is a retrovirus encoding structural genes and, like human immunodeficiency virus and human T ceU leukemia virus I, several anciUary reading frames collectively termed the belgenes. We have previously shown that HFV transgenic mice develop an encephalopathy with neuronal loss in hippocampus and cerebral cortex. We have now raised and characterized rabbit antisera to various recombinant portions of gag, pot, env, and bel-I, the viraltransactivator. Immunoreactivity for gag and bel-I was observed in nuclei and processes of hippocampal and cortical neurons before the onset of morphological lesions and correlated with the appearance of HFV mRNA. Astrocyte-derived multinucleated giant ceUs containing HFV proteins were present in the brain oftransgenic mice coexpressingfuU- length HFV genes but not in mice expressing truncated gag and env, suggesting that these genes contain afusogenic domain. Expression of fuU-length structural genes decreased the life expectancy oftransgenic mice, implying an a4Juvant rolefor these proteins in HFV-induced brain damage. (Am] Pathol 1993, 142:1061-1072)}, subject = {Molekularpathologie}, language = {en} } @article{RethwilmErlweinBaunachetal.1991, author = {Rethwilm, Axel and Erlwein, Otto and Baunach, Gerald and Mauerer, Bernd and ter Meulen, Volker}, title = {The transcriptional transactivator of human foamy virus maps to the bel 1 genomic region}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47342}, year = {1991}, abstract = {The human foamy virus (HFV) genome possesses three open reading frames (bel I, 2, and 3) located between env and the 3' long terminal repeat. By analogy to other human retroviruses this region was selected as the most Iikely candidate to encode the viral transactivator. ResuIts presented here confirmed this and showed further that a deletion introduced only into the bell open reading frame of a plasmid derived from an infectious molecular clone of HFV abolished transactivation. In contrast, deletions in bel 2 and bel 3 had only minor effects on the ability to transactivate. The role of the bel I genomic region as a transactivator was further investigated by eukaryotic expression of a genome fragment of HFV spanning the bel I open reading frame. A construct expressing bell under control of a heterologous promoter was found to transactivate the HFV long terminal repeat in a dose-dependent fashion. Furthermore, it is shown that the U3 region of the HFV long terminal repeat is sufficient to respond to the HFV transactivator.}, subject = {Virologie}, language = {en} } @article{LiebertSchneiderSchauliesterMeulen1988, author = {Liebert, U. G. and Schneider-Schaulies, Sibylle and ter Meulen, V.}, title = {Measles Virus infections of the central nervous system (CNS) of rats}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-34087}, year = {1988}, abstract = {No abstract available}, subject = {Masernvirus}, language = {en} } @article{SchneiderSchauliesLiebertBaczkoetal.1988, author = {Schneider-Schaulies, Sibylle and Liebert, U. G. and Baczko, K. and ter Meulen, Volker}, title = {Molecular Biological Analyses of Measles Virus Gene Expression in the CNS of Acutely and Persistently Infected Rat Brain Cells}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-34104}, year = {1988}, abstract = {No abstract available}, subject = {Masernvirus}, language = {en} } @article{KerkauSchmittLandgrafSchimpletal.1989, author = {Kerkau, Thomas and Schmitt-Landgraf, Renate and Schimpl, Anneliese and Wecker, Eberhard}, title = {Downregulation of HLA Class I Antigensin HIV-1-Infected Cells}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47172}, year = {1989}, abstract = {By means of indirect immunofluorescence analysis we investigated the effect of HIV -1 infection on HLA class I surface antigens. We report here that in CD4\(^+\) HeLa cells, in H9 cells, and in peripheral T Iymphocytes HLA class I antigens are down regulated following infection with HIV -1. The downregulation is effected at a posttranscriptional level since the amounts of HLA class I specific mRNA are similar in infected and uninfected cells. This phenomenon is not only correlated with the state of infection, that is, the presence of P24 of HIV-l in the cells, but also depends on the time of infection. Upon HLA class I downregulation by HIV infection, the specific lysis of peripheral blood cells by allogeneic CTL is reduced.}, language = {en} } @article{BrabletzPfeufferSchorretal.1993, author = {Brabletz, Thomas and Pfeuffer, Isolde and Schorr, Elke and Siebelt, Friederike and Wirth, Thomas and Serfling, Edgar}, title = {Transforming growth factor \(\beta\) and cyclosporin A inhibit the inducible activity of the interleukin-2 gene in T cells through a noncanonical octamer-binding site}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31199}, year = {1993}, abstract = {Transforming growth factor \(\beta\) (TGF-\(\beta\)) has a growth-inhibitory effect on numerous different cell types of the immune system, including T lymphocytes. We show in this study that the inhibitory action of TGF-\(\beta\) on T lymphocytes is accompanied by a block of interleukin 2 (IL-2) gene expression which is mediated, at least in part, by inhibition of IL-2 promoter/enhancer activity. The functional analysis of cis-regulatory (protoenhancer) elements of the IL-2 enhancer/promoter region showed that the most TGF-\(\beta\)-responsive element maps to its so-called upstream promoter site. The proto-enhancer activity of the upstream promoter site element is also inhibited by cyclosporin A. The upstream promoter site DNA harbors two noncanonical, closely linked binding sequences for octamer and AP-1-like factors. Both sites are involved in the establishment of IL-2 enhancer activity. Since the activity of genuine octamer sites but not that of AP-1-binding sites is also impaired by TGF-\(\beta\) and cyclosporin A in E14 T lymphoma cells, we conclude that both immunosuppressives interfere with the activity but not the DNA binding of octamer factors in T lymphocytes.}, language = {en} } @article{MuellerKrennSchindleretal.1993, author = {M{\"u}ller, J. G. and Krenn, V. and Schindler, C. and Czub, S. and Stahl-Henning, C. and Coulibaly, C. and Hunsmann, G. and Kneitz, C. and Kerkau, Thomas and Rethwilm, Axel and terMeulen, Volker}, title = {Alterations of thymus cortical epithelium and interdigitating dendritic cells but no increase of thymocyte cell death in the early course of simian immunodeficiency virus infection}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-32583}, year = {1993}, abstract = {No abstract available}, language = {en} } @article{KneitzKerkauMuelleretal.1993, author = {Kneitz, Christian and Kerkau, Thomas and M{\"u}ller, Justus and Coulibaly, Cheick and Stahl-Henning, Christiane and Hunsmann, Gerhard and H{\"u}nig, Thomas and Schimpl, Anneliese}, title = {Early phenotypic and functional alterations in lymphocytes from simian immunodeficiency virus infected macaques}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-32593}, year = {1993}, abstract = {Phenotypic and functional changes in lymphocytes from rhesus monkeys (Macaca mulatta) were investigated during the first 6 months after infection with SIVmac 32H. Animals preimmunized with keyhole limpet hemocyanin (KLH) were sacrificed l, 3, 6, 12, and 24 weeks post infection. Subset composition and function of lymphocytes from blood, spleen, lymph node and thymus were analysed. In addition to a rapid decline in CD4/CD8 ratios, a massive reduction in CD29+CD4+ cells was seen in the periphery. Although depletion of this subset was observed throughout the course of this experiment, the loss of proliferative T cell responses was most pronounced very early after infection and partially recovered after Month 3. Polyclonal cytotoxic responses were only slightly affected. In the thymus, a gradual, but moderate loss of CD4 + CD8 + immature thymocytes, and a relative increase in both CD4 + and CD8 + mature subsets was observed. Infectious virus was readily recovered from homogenates of lymph node and spleen, but not of thymus tissue. Interestingly, however, virus was detected in thymocytes from all infected animals by cocultivation with a simian immunodeficiency virus (SIV) susceptible cell line.}, language = {en} }