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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 41 (1995), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In African trypanosomiasis the occurrence of antibodies to interferon-γ (IFN-γ) was studied in both humans and experimental rats. Sera from patients infected with Trypanosoma brucei gambiense showed increased levels of antibodies to IFN-γ as compared with controls from the same regions in Africa. In Sprague-Dawley rats infected with Trypanosoma brucei brucei an early appearance of IFN-γ-producing spleen cells was observed, followed by an increase in levels of antibodies against IFN-γ in the sera. Previously, IFN-γ has been found to play a crucial role in trypanosome infections in rats by promoting proliferation of Trypanosoma brucei brucei. The appearance of antibodies to IFN-γ in humans, as in rats, indicates that this cytokine is produced also in the human infection. Its parasitic growthstimulating and pathophysiological effects on the organism may be reduced by the antibodies.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A protein factor that stimulates CD8+ lymphocytes to produce and secrete IFN-γ has been purified from Trypanosoma brucei brucei (T.b. brucei). This was accomplished by raising monoclonal antibodies (MoAbs) against a fraction of T.h. brucei obtained by gel filtration, whieh contained high levels of material inducing rat mononuelear cells (MNC) to IEN-y production. MoAbs from four hybridomas strongly inhibited trypanosome-induced IFN-γ production. One of them (MO1) was used for purification of the trypanosome-derived lymphocyte triggering factor (TLTF) by affinity chromatography, SDS electrophoresis of the purified TLTF displayed a band of 42-45 kDa MW. Gel filtration of homogenates of whole parasites yielded several peaks of IFN-γ-inducing activity with a lowest MW of 41 46 kDa. Bioactivity of all peaks was blocked by MO1. suggesting that a single molecule, or a single epitope of additional molecules, is responsible for the different peaks with IFN-γ-indueing activity. IFN-γ released from MNC stimulates T.b. brucei growth. Blocking of TLTF in vitro with MO1 inhibited MNC-supported growth of the parasites. To study the in vivo relevance of TLTF in the course of experimental African trypanosomiasis, MO1 was used to treat rats and mice at different times after infection. Treatments instituted at different time-points after infection suppressed parasite growth, abrogated the IFN-γ production by splenocytes indueed by the infection and prolonged survival of the animals. The data support the hypothesis that TLTF and IFN-γ have a erueial regulatory function in the parasite host interactions and that these moleeules influence the disease eourse during experimental African trypanosomiasis.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: CDS+ T cells can perform both Th1 - and Th2-like functions by producing cytokines such as interferonγ (IFN-γ) and interleukin-4 (IL-4), as well as the immune response down-regulating transforming growth factor-β (TGF-β), which are all involved in the development of experimental autoimmune myasthenia gravis (EAMG), a model for human MG. We have reported that depletion of CD8+ T cells results in the suppression of EAMG accompanied by the down-regulation of AChR-specific B cell responses and AChR-reactive IFN-γ secreting Th1-like cells. To identify the involvement of IFN-γ, IL-4 and TGF-β in the development of EAMG after CD8+ T cell depletion, the expression of mRNA for these cytokines was studied in mononuclear cells from popliteal, inguinal and mesenteric lymph nodes, spleen and thymus by adopting in situ hybridization with complementary DNA oligonucleotide probes. Depletion of CD8+ T cells resulted in decreased levels of IFN-7 and IL-4 mRNA expressing cells in different lymphoid organs except thymus, but no change in the numbers of TGF-β mRNA expressing cells. The results imply that the suppression of EAMG after depletion of CD8+ T cells is caused by decreasing the effector factors but not by increasing the suppressor factor(s).
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Parasitology Today 8 (1992), S. 237-239 
    ISSN: 0169-4758
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurocytology 21 (1992), S. 846-852 
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The extracellular haemoflagellateTrypanosoma brucei brucei releases a factor, which can induce CD8+ T-cells to produce interferon-γ. Interferon-γ derived from these cells promotes proliferation of the trypanosomes. We now report that these trypanosomes can interact with small neurons in cultures of rat dorsal root ganglia, which contain an interferon-γ like immunoreactive molecule. Cultures of dorsal root ganglia were able to promote the proliferation and survival of the trypanosomes and this growth promoting effect was blocked by monoclonal antibodies against the trypanosome-derived lymphocyte triggering factor, interferon-γ and CD8+ and by Fab-fragments of these antibodies. Living trypanosomes and the factor induced an increase in expression of major histocompatibility complex class I antigens in the cultures; this induction was blocked by Fab fragments of the interferon-γ antibody, indicating that it is mediated by release of the neuronal interferon-γ-like immunoreactive molecule. These data suggest, that the interferon-γ-like immunoreactive molecule in small dorsal root ganglion neurons mimicks certain physiological effects of lymphocyte derived interferon-γ. Furthermore, the trypanosomes and small sensory neurons seem to interact bidirectionally by release of the trypanosome-derived lymphocyte triggering factor and the neuronally derived interferon-γ-like molecule, whereby, perhaps, neuronal disturbances may be elicited and trypanosome proliferation regulated.
    Type of Medium: Electronic Resource
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