Publications
126 results found
Antoniazi S, Price HP, Kropf P, et al., 2004, Chemokine gene expression in toll-like receptor-competent and -deficient mice infected with <i>Leishmania major</i>, INFECTION AND IMMUNITY, Vol: 72, Pages: 5168-5174, ISSN: 0019-9567
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- Citations: 35
Kropf P, Freudenberg N, Kalis C, et al., 2004, Infection of C57BL/1 OScCr and C57BL/1 OScNCr mice with <i>Leishmania major</i> reveals a role for Toll-like receptor 4 in the control of parasite replication, JOURNAL OF LEUKOCYTE BIOLOGY, Vol: 76, Pages: 48-57, ISSN: 0741-5400
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- Citations: 74
Kropf P, Freudenberg MA, Modolell M, et al., 2004, Toll-like receptor 4 contributes to efficient control of infection with the protozoan parasite <i>Leishmania major</i>, INFECTION AND IMMUNITY, Vol: 72, Pages: 1920-1928, ISSN: 0019-9567
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- Citations: 204
Kropf P, Herath S, Weber V, et al., 2003, Factors influencing <i>Leishmania major</i> infection in IL-4-deficient BALB/c mice, PARASITE IMMUNOLOGY, Vol: 25, Pages: 439-447, ISSN: 0141-9838
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- Citations: 36
Herath S, Kropf P, Müller I, 2003, Cross-talk between CD8<SUP>+</SUP> and CD4<SUP>+</SUP> T cells in experimental cutaneous leishmaniasis:: CD8<SUP>+</SUP> T cells are required for optimal IFN-γ production by CD4<SUP>+</SUP> T cells, PARASITE IMMUNOLOGY, Vol: 25, Pages: 559-567, ISSN: 0141-9838
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- Citations: 37
Kropf P, Herath S, Klemenz R, et al., 2003, Signaling through the T1/ST2 molecule is not necessary for Th2 differentiation but is important for the regulation of type 1 responses in nonhealing <i>Leishmania major</i> infection, INFECTION AND IMMUNITY, Vol: 71, Pages: 1961-1971, ISSN: 0019-9567
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- Citations: 29
Kropf P, Freudenberg M, Modolell M, et al., 2003, Bone marrow macrophages from TLR4-deficient mice display an impaired capacity to control the replication of Leishmania major parasites, 17th Meeting of the EMDS
Kropf P, Muller I, 2003, IL-4 Knock-out mice, Cytokine Knockouts, 2nd Edition, Editors: Fantuzzi, Totowa, New Jersey, USA, Publisher: Humana Press, Pages: 187-202
Herath S, Kropf P, Muller I, 2003, Cross talk between CD8+ and CD4+ T cells in experimental leishmaniasis: CD8+ T cells are required for optimal IFN-gamma production by CD4+ T cells., Parasite Immunology, Vol: 25, Pages: 559-2567
Kropf P, Freudenberg M, Modolell M, et al., 2003, Toll-like receptor 4 contributes to the efficient control of infection with the protozoan parasite Leishmania major, International Cytokine Society
Kropf P, Herath S, Tewari R, et al., 2002, Identification of two distinct subpopulations of <i>Leishmania major</i>-specific T helper 2 cells, INFECTION AND IMMUNITY, Vol: 70, Pages: 5512-5520, ISSN: 0019-9567
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- Citations: 13
Kropf P, Bickle Q, Herath S, et al., 2002, Organ-specific distribution of CD4<SUP>+</SUP> T1 /ST2<SUP>+</SUP> Th2 cells in <i>Leishmania major</i> infection, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 32, Pages: 2450-2459, ISSN: 0014-2980
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- Citations: 21
Kropf P, Herath S, Bickle Q, et al., 2002, Organ-specific distribution and cytokine production of CD4* T 1/ST2+ T cells in Leishmania major infected mice, Immunoparasitology Meeting
Herath S, Kropf P, Muller I, 2002, Cross-talk between CD8* and cells in experimental cutaneous leishmaniasis, Immunoparasitology Meeting
Muller I, Herath S, Kropf P, 2002, Ageing alters the course of nonhealing Leishmania major infections in IL-4 deficient BALB/c mice, Immunoparasitology Meeting
Kropf P, Herath S, Klemenz R, et al., 2002, Signalling through the T1/ST2 molecule is not necessary for Th2 differentiation, but is important for the regulation of type 1 responses in nonhealing Lesmania major infection, British Society for Parasitology, Trypanosomiasis and Leishmaniasis seminar
Roe T, Lukey P, Muller I, et al., 2002, TGF-beta and mycobacterial infection, 5th International Congress on the Pathogenesis of Mycobacterial infections
Kropf P, Müller I, Brunson K, 2002, The leishmaniasis model, IMMUNOLOGY OF INFECTION, SECOND EDITION, Vol: 32, Pages: 463-492, ISSN: 0580-9517
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- Citations: 3
Kropf P, Brunson K, Muller I, 2002, The Leishmaniasis Model, Immunology of Infection, part of Methods in Microbiology Series, 2nd Edition, Editors: SHE, Kabelitz, London, Publisher: Academic Press Ltd, Pages: 463-492
Marshall BG, Kropf P, Murray K, et al., 2000, Bronchopulmonary and mediastinal leishmaniasis:: An unusual clinical presentation of <i>Leishmania donovani</i> infection, CLINICAL INFECTIOUS DISEASES, Vol: 30, Pages: 764-769, ISSN: 1058-4838
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- Citations: 19
Kropf P, Schopf LR, Chung CL, et al., 1999, Expression of Th2 cytokines and the stable Th2 marker ST2L in the absence of IL-4 during <i>Leishmania major</i> infection, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 29, Pages: 3621-3628, ISSN: 0014-2980
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- Citations: 39
Etges R, Müller I, 1998, Progressive disease or protective immunity to <i>Leishmania major</i> infection:: the result of a network of stimulatory and inhibitory interactions, JOURNAL OF MOLECULAR MEDICINE-JMM, Vol: 76, Pages: 372-390, ISSN: 0946-2716
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- Citations: 37
Kropf P, Muller I, Brunson K, et al., 1998, The Leishmaniasis model, METHODS IN MICROBIOLOGY, VOL 25, Vol: 25, Pages: 419-458, ISSN: 0580-9517
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- Citations: 15
Kropf P, Etges R, Schopf L, et al., 1997, Characterization of T cell-mediated responses in nonhealing and healing Leishmania major infections in the absence of endogenous IL-4., J Immunol, Vol: 159, Pages: 3434-3443, ISSN: 0022-1767
IL-4 drives polarized Th2 responses, and differentiating Th2 cells down-regulate their sensitivity to IL-12. Therefore, the failure of BALB/c mice to heal Leishmania major infection could be due to an IL-4-dependent biased Th2 response or to a reduced capacity of Leishmania-specific Th cells to respond to IL-12. We examined the ability of CD4+ Th cells from L. major-infected wild-type and IL-4-deficient BALB/c mice to respond to IL-12. We show that the inability of normal and IL-4-deficient BALB/c mice to heal L. major infections is due to their inability to generate effective Th1 responses and not to persistent IL-4-dominated Th2 responses. Redirection of immune responses in vivo by administration of IL-12 or anti-CD4 mAb treatment in the early phase of infection (+/-12 days) allows both normal and IL-4-deficient BALB/c mice to heal their lesions by allowing them to develop an efficient Th1 response regardless of the presence or the absence of IL-4. Finally, on a population level, Ag-specific Th cells from infected animals induced to heal display a strongly elevated response to IL-12.
Müller I, Freudenberg M, Kropf P, et al., 1997, Leishmania major infection in C57BL/10 mice differing at the Lps locus: a new non-healing phenotype., Med Microbiol Immunol, Vol: 186, Pages: 75-81, ISSN: 0300-8584
The course of cutaneous leishmaniasis was examined in mice from two genetically closely related strains, C57BL/10ScCr (Cr) and C57BL/10ScSn (Sn). Sn mice are able to heal Leishmania major infections, while Cr mice are unable to heal. The cutaneous lesions of the Cr mice progressed continuously and the increase in lesion size was paralleled by an unrestricted growth of the parasites in vivo. Cr mice, in contrast to their Sn counterparts, are highly resistant to all effects of lipopolysaccharide (LPS). The nonhealing L. major infection in Cr mice is in sharp contrast to the course of infection in another endotoxin-nonresponder mouse strain, C3H/HeJ, which heal infections with L. major. Cr mice exhibit, in addition to the defective LPS responsiveness, an impaired interferon-gamma (IFN-gamma) response after infection with a variety of microorganisms. The insufficient activation of parasitized macrophages to kill intracellular L. major could be due to the inability of splenocytes from infected Cr mice to secrete IFN-gamma upon restimulation with L. major. IFN-gamma is essential for the efficient activation of parasitized macrophages to kill intracellular L. major by producing nitric oxide (NO). Although bone marrow-derived Cr macrophage do not produce NO in response to LPS, both Sn and Cr macrophages release NO upon stimulation with IFN-gamma and tumor necrosis factor, indicating that they are responsive to activation by these cytokines.
Noben-Trauth N, Kropf P, Müller I, 1996, Susceptibility to Leishmania major infection in interleukin-4-deficient mice., Science, Vol: 271, Pages: 987-990, ISSN: 0036-8075
Interleukin-4 (IL-4), a pleiotropic cytokine, is a major regulator of the immune system and is considered crucial for the development of T helper cell type 2 (TH2) responses. The susceptibility of BALB/c mice to infection with Leishmania major has been associated with a polarized TH2 response and an inability to down-modulate IL-4 production. The role of IL-4 in vivo was examined directly by disrupting the IL-4 gene in BALB/c embryonic stem cells. Despite the absence of IL-4, the genetically pure BALB/c mutant mice remained susceptible to L. major infection, showed no signs of lesion healing or parasite clearance, and did not switch to a TH1 phenotype.
Kantengwa S, Müller I, Louis J, et al., 1995, Infection of human and murine macrophages with Leishmania major is associated with early parasite heat shock protein synthesis but fails to induce a host cell stress response., Immunol Cell Biol, Vol: 73, Pages: 73-80, ISSN: 0818-9641
Heat shock/stress proteins (HSP) represent the most conserved proteins expressed in prokaryotes and eukaryotes. These constitutive and inducible proteins function as molecular chaperones and are part of virulence factors. They participate in self/non-self discrimination and may protect phagocytes from the toxic effects of the reactive oxygen species generated by these cells during bacterial phagocytosis and infection. In this study, we investigated the early stress response of host cells [either human alveolar macrophages (AM) or murine peritoneal macrophages (PM)] during infection by an obligate intracellular parasite (Leishmania major), which lives within phagolysosomes. Immunoblotting with specific antibodies demonstrated that L. major had no effect on host stress protein synthesis, but synthesized high levels of its own stress proteins within AM and PM. The lack of induction of a host cell stress response may relate to the failure of L. major to activate the respiratory burst in these cells, whereas the upshift of L. major HSP within macrophages is part of an adaptive response of the parasite to the host.
Müller I, Kropf P, Louis JA, et al., 1994, Expansion of gamma interferon-producing CD8+ T cells following secondary infection of mice immune to Leishmania major., Infect Immun, Vol: 62, Pages: 2575-2581, ISSN: 0019-9567
Reinfection of immune mice with Leishmania major elicits a secondary gamma interferon (IFN-gamma) response to which specific CD8+ T cells are essential. We have shown previously that specific CD8+ T cells from reinfected immune mice release substantially higher levels of IFN-gamma, a cytokine essential for the efficient activation of parasitized macrophages to kill intracellular L. major. By using an ELISPOT assay, which allows the detection of IFN-gamma production by individual cells, it is shown here that this elevated IFN-gamma response is the result of an increase of up to 50-fold in the frequency of parasite-specific CD8+ T lymphocytes in the spleens and draining lymph nodes of both immune reinfected CBA and BALB/c mice. This observation is additional evidence of the role that CD8+ T cells play in immunity to reinfection with L. major.
de Kossodo S, Grau GE, Louis JA, et al., 1994, Tumor necrosis factor alpha (TNF-alpha) and TNF-beta and their receptors in experimental cutaneous leishmaniasis., Infect Immun, Vol: 62, Pages: 1414-1420, ISSN: 0019-9567
Experimental infection of BALB/c mice with Leishmania major leads to lesions which progress without healing and visceralization, reproducing the most severe forms of human leishmaniasis, while resistant mice like CBA spontaneously resolve lesions and develop protective immunity. Given the conflicting data pertaining to the role of tumor necrosis factor alpha (TNF) in Leishmania infection, we analyzed the expression of TNF, tumor necrosis factor beta (lymphotoxin), and TNF receptor type I (TNF-RI) and type II (TNF-RII) genes in vivo and correlated TNF gene expression in vivo with the production of biologically active TNF by lymphoid cells in vitro. No significant difference in the expression of TNF mRNA was found between susceptible and resistant strains of mice during the course of infection. The depletion of CD4+ T cells in vitro did not change the level of TNF mRNA in BALB/c lymph node cells but led to the total disappearance of TNF mRNA in CBA mice. Unprimed spleen cells did not produce detectable amounts of TNF, whereas 1 week after infection, TNF bioactivity was detected and increased in both strains of mice until 5 weeks of infection. While neutralization of TNF activity in vivo did not alter the course of infection in BALB/c mice, in CBA mice it led to an increase in lesion size and a delay in the healing process but did not interfere significantly with the outcome of infection. Finally, no significant difference in the levels of lymphotoxin, TNF-RI, or TNF RII mRNA expression was found between both strains. The information resulting from these investigations supports the notion that, in vivo, TNF is not the decisive factor responsible for the resistant versus susceptible phenotype in leishmania infection.
Stefani MM, Müller I, Louis JA, 1994, Leishmania major-specific CD8+ T cells are inducers and targets of nitric oxide produced by parasitized macrophages., Eur J Immunol, Vol: 24, Pages: 746-752, ISSN: 0014-2980
Lines of Leishmania major-specific CD8+ T cells were derived from the lymph nodes and spleens of CBA mice, immune following resolution of a primary infection, 7 days after secondary challenge with viable L. major. Specific stimulation of these CD8+ T cells by bone marrow-derived macrophages infected with L. major led to the release of interferon-gamma by CD8+ T cells and nitric oxide by macrophages. Interestingly, the nitric oxide released by bone marrow-derived macrophages down-regulated the production of interferon-gamma by specifically activated CD8+ T cells. The proliferation and long-term maintenance of these parasite-specific CD8+ T cells was impaired by the nitric oxide produced by stimulating infected macrophages as a result of cytokines released by activated stimulating infected macrophages as a result of cytokines released by activated CD8+ T cells. Taken together, the results indicate that L. major-specific CD8+ T cells are sensitive to the toxic effect of the nitric oxide that they induce.
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