@article{HackerSchmidtHughesetal.1985,
  author    = {Hacker, J{\"o}rg and Schmidt, G. and Hughes, C. and Knapp, S. and Marget, M. and Goebel, W.},
  title     = {Cloning and characterization of genes involved in the production of mannose-resistant, neuraminidase-susceptible (X) fimbriae from an uropathogenic O6:K15:K31 Escherichia coli strain},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59353},
  year      = {1985},
  abstract  = {The Qropathogenic Escherichia coli strain 536 (06:K15:H31) exhibits a mannose-resistant hemagglutination phenotype (Mrh) with bovine erythrocytes and delayed Mrh with human and guinea pig erythrocytes. Neuraminidase treatment of the erythrocytes abolishes mannose resistant hemagglutination, which is typical for X fimbriae. E. coli strain 536 synthesizes two different fimbriae (Fim phenotype) prQtein subunits, 16.5 and 22 kilodaltons in size. In addition the strain shows mannose-sensitive hemagglutination and common type I (Fl) fimbriae. The cosmid clone E. coli K-12(pANN801) and another nine independently isolated Mrh+ cosmid clones derived from a cosmid gene bank of strain 536 express the 16.5-kilodalton protein band, bot not the 22-kilodalton protein, indicating an association of the Mrh+ property with the "16.5-kilodalton fimbriae." All cosmid clones were fimbriated, and they reacted with antiserum produced against Mrh+ fimbriae of the E. coli strain HB101(pANN801) and lacked mannose-sensitive hemagglutination (Fl) funbriae. From the Mrh fim cosmid DNA pANN801, several subclones coding for hemagglutination and X fimbriae were constructed. Subclones that express both hemagglutination and fimbriae and subclones that only code for the hemagglutination antigen were isolated; subclones that only produce fimbriae were not detected. By transposon Tn5 mutagenesis we demonstrated that about 6.5 kilobases of DNA is required for the Mrh+ Fim+ phenotype, and the 1.5- to 2-kilobase DNA region coding for the structural proteiil of the fimbriae has been mapped adjacent to the region responsible for the Mrh+ phenotype. Two different regions can thus be distinguished in the adhesion determinant, one coding for hemagglutination and the other coding for fimbria formation. Transformation of plasmid DNA from these subclones into a Mrh- Fim- mutant of E. coli 536 and into a galE (rough) strain of Salmonella typhimurium yielded transformants that expressed both hemagglutination and fimbria production.},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{HughesHackerRobertsetal.1983,
  author    = {Hughes, C. and Hacker, J{\"o}rg and Roberts, A. and Goebel, W},
  title     = {Hemolysin production as a virulence marker in symptomatic and asymptomatic urinary tract infections caused by Escherichia coli},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59346},
  year      = {1983},
  abstract  = {Potential virulence, as defined by combined Ievels of adhesion to urinary epithelial cells, serum resistance, and mouse toxicity, was assessed for Escherichia coli strains causing symptomatic and asymptomatic urinary tract infections in relation to the carriage of hemolysin and other suspected virulence determinants. Hemolysin production (Hly), associated with certain 0 (04, 06, 018, and 075), K (5), and hemagglutination (VI and VII) antigenic types but not colicin V production (Cva), was evident in 83 and 60\% ofisolates in groups possessing high potential virulence andin only 11 and 6\% of those with low virulence. Strains of particular 0-types were not more virulent per se, but among the serotypes, specific combinations of virulence factors appeared decisive, e.g., 018 HAVI B/D/G Hly+ K5+t- and 018 HAIIIIIVBN Hly- Cva +t- Kl +t- strains were, respectively, of high and low potential virulence. Isolates with high potential virulence were found to a similar extent in symptomatic and asymptomatic infections.},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{HackerHughesHofetal.1983,
  author    = {Hacker, J{\"o}rg and Hughes, C. and Hof, H. and Goebel, W.},
  title     = {Cloned hemolysin genes from Escherichia coli that cause urinary tract infection determine different levels of toxicity in mice},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59330},
  year      = {1983},
  abstract  = {After intraperitoneal injection of mice with Escherichia coli strains isolated from patients with urinary tract infections, the mortality due to hemolytic (Hly+) and nonhemolytic (Hiy-) isolates was 77 and 40\%, respectively. Deletion of the chromosomal hemolysin (h/y) determinant in an E. co/i 06:K15:H31 urinary tract infection strain led to a significant reduction in toxicity for mice, and its reintroduction on a recombinant plasmid partially restored the original toxicity. Although introduction of the cloned plasmid pHiy152-encoded hly determinant into the Hly- E. coli 06 mutant strain increased toxicity by only a marginal degree, transformation with the cloned chromosomal hly determinants from two E. coli strains of serotypes 018ac:K5:H- and 075:K95:H? resulted in markedly greater toxicity, even exceeding that of the original Hly+ E. coli 06 wild-type strain.},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{HughesHackerDueveletal.1987,
  author    = {Hughes, C. and Hacker, J{\"o}rg and D{\"u}vel, H. and Goebel, W},
  title     = {Chromosomal deletions and rearrangements cause coordinate loss of hemolysis, fimbriation and serum resistance in an uropathogenic strain of Escherichia coli},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-59470},
  year      = {1987},
  abstract  = {No abstract available},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{MollMitchellMcConvilleetal.1989,
  author    = {Moll, Heidrun and Mitchell, Graham F. and McConville, Malcom J. and Handman, Emanuela},
  title     = {Evidence for T cell recognition in mice of a purified lipophosphoglycan from Leishmania major},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61288},
  year      = {1989},
  abstract  = {We have previously reported that a Leishmania major lipophosphoglycan (LPG), given with killed Corynebacterium parvum as an adjuvant, can vaccinate mice against cutaneous leishmaniasis. In order to analyze whetber T cells are able to recognize this important parasite antigen, we have studied both humoral and cellular immune responses to L. major LPG that bad been isolated from promastigotes by sequential solvent extraction and bydrophobic chromatography. The data sbow that immunization of mice with highly purified LPG induced an increase in frequency of L. major-reactive T cells and the production of immunoglobulin G antibodies to LPG. Furthermore, genetically resistant mice infected with L. major were able to develop a specific delayed-type hypersensitivity response in the ear to L. major LPG. These findings strongly suggest that T cells can recognize and respond to glycolipid antigens, in this case a bost-protective Leishmania LPG, even though such antigens appear not to be potent T-cell stimulators in mice.},
  subject      = {Biologie},
  language  = {en}
}
@article{MollScollay1989,
  author    = {Moll, Heidrun and Scollay, Roland},
  title     = {L3T4+ T cells promoting susceptibility to murine cutaneous leishmaniasis express the surface marker Ly-24 (Pgp-1)},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61275},
  year      = {1989},
  abstract  = {No abstract available},
  subject      = {Biologie},
  language  = {en}
}
@article{MollScollayMitchell1988,
  author    = {Moll, Heidrun and Scollay, R. and Mitchell, G. F.},
  title     = {Resistance to cutaneous leishmaniasis in nude mice injected with L3T4+ T cells but not with Ly-2+ T cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61269},
  year      = {1988},
  abstract  = {No abstract available},
  subject      = {Biologie},
  language  = {en}
}
@article{KramerBinningerSchirrmacheretal.1986,
  author    = {Kramer, Michael D. and Binninger, Linda and Schirrmacher, Volker and Moll, Heidrun and Prester, Marlot and Nerz, Gaby and Simon, Markus M.},
  title     = {Characterization and isolation of a trypsin-like serine protease from a long-term culture cytolytic t cell line andits expression by functionally distinct T cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31636},
  year      = {1986},
  abstract  = {No abstract available},
  subject      = {Biologie},
  language  = {en}
}
@article{SimonNerzPresteretal.1985,
  author    = {Simon, M. M. and Nerz, G. and Prester, M. and Moll, Heidrun},
  title     = {Immunoregulation by mouse T cell clones III. Cloned H-Y-specific cytotoxic T cells secrete a soluble mediator(s) that inhibits cytotoxic responses by acting on both Lyt-2\(^-\) and L3T4\(^-\)- lymphocytes},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31625},
  year      = {1985},
  abstract  = {In this study we report that cloned Thy-l +, L3T4-, Lyt-l-, Lyt-2+, H-Y-specific and H-2Db-restricted cytotoxic T ce11 lines (CTLL) when indueed by lectin or antigen secrete a soluble mediator(s) (SF) that inhibits proliferation and generation of cytotoxic lymphocytes (CTL) in mixed lymphocyte cultures (MLC). The biological activity was separable by gel filtration and appeared as a broad peak in the moleeular mass range between 10000 and 50000 kDa. It was found that the suppressive activity released by CTLL neither strictly correlates with their cytotoxic potential nor with their ability to produce immune interferon or Iymphotoxin. SF was shown to elicitits activity in an antigen-nonspeeific manner in that it suppressed the maturation of T lymphocytes responding to both, the appropriate H-Y antigen as weH as to unrelated H_2d alloantigens or to the hapten 2,4,6-trinitrophenyl (TNP). The effect of SF on CTL responses was most pronounced in early phases of primary or secondary MLC. When analyzed for its inhibitory activity on precursor ceHs in populations selected for either Lyt-2- or L3T4- lymphocytes, it was found that SF interfered with the maturation of both subsets. The inhibition of CTL responses elicited by SF could not be reversed by the addition of exogenous interleukin 2. The findtng that SF also inhi. bited the proliferation of some but not a11 antigen-dependent cloned T ceHs with helper or eytc'toxic potential provides evidence that the faetor also may regulate effector lymphl)cytes. In addition, the results support the assumption that SF exerts its effect direetly on the responder rather than the stimulator population, and demonstrate that the development of CTL from their preeursor eeHs is contro11ed at least in part by the eytotoxic effeetor cells themselves via a soluble factor(s) that interferes with distinct stages of T ce11 maturation. These findings again emphasize the expression of multiple functions by CTL and indieate their possible role du ring the course of an immune response by their capability to eliminate target cells and to secrete a soluble product(s) that mediates feedback contro!.},
  subject      = {Infektionsbiologie},
  language  = {en}
}
@article{BogdanMollSolbachetal.1990,
  author    = {Bogdan, Christian and Moll, Heidrun and Solbach, Werner and R{\"o}llinghoff, Martin},
  title     = {Tumor necrosis factor-\(\alpha\) in combination with interferon-\(\gamma\), but not with interleukin 4 activates murine macrophages for elimination of Leishmania major amastigotes},
  volume    = {20},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31614},
  pages     = {1131 -- 1135},
  year      = {1990},
  abstract  = {We have previously shown that during an infection with Leishmania major, susceptible BALB/c mice, as opposed to mice of a resistant strain (C57BLl6), are primed by lipopolysaccharide for the production of high levels of tumor necrosis factor-\(\alpha\) (TNF-\(\alpha\)) which is known to be a potent maerophage M\(\Phi\) stimulator in other parasitic diseases. In the present study we investigated whether TNF-\(\alpha\) activates M\(\Phi\) for killing of L. major parasites. In the absence of interferon-y (IFN-\(\gamma\)) or lipopolysaccharide, TNF-\(\alpha\) (0.025-25000 U/ml) failed to activate peritoneal exudate M\(\Phi\) from BALB/c mice for killling of L. major amastigotes. In the presence of suboptimal doses of IFN-\(\gamma\) (5 or 10 Vlml), however, TNF-\(\alpha\) mediated a rapid elimination of intracellular parasites, which was highly significant compared to IFN-\(\gamma\) alone. Tbe combination of TNF with interleukin 4, in contrast, was inactive in this respect and allowed survival of intracellular parasites. From these data we conelude that the presence of IFN-\(\gamma\) is crucial for TNF-\(\alpha\)-mediated killing of L. major parasites by M\(\Phi\). Disease progression in susceptible mice therefore seems to be a consequence of a deficiency of IFN-\(\gamma\) and a predominance of interleukin 4 rather than the result of an excess amount of TNF-\(\alpha\).},
  subject      = {Infektionsbiologie},
  language  = {en}
}