Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Peripheral T-cell tolerance: the contribution of permissive T-cell migration into parenchymal tissues of the neonate (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 169 (1999), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: T lymphocytes with self-destructive capacity are often found in healthy individuals, indicating efficient control mechanisms chat prevent chronic autoimmune deseases. Since naive T lymphocytes do not circulate through extralymphoid tissues the concept has emerged that peripheral T cells ignore tissue-,specific antigens unless they are presented by professional antigen-presenting cells in the lymphoid compartments. However, this view pays attention only to experiments performed in adult animals. This report reviews the evidence that tissues of neonatal mice, in contrast to adults, exhibit high accessibility for naive T cells, thereby allowing the direct contact with tissue-specific self-antigens on parenchymal cells during neonatal life and tolerance induction to such self-antigens. In mouse bone marrow chimeras generated at different ages, recent thymic emigrants were tolerized to a major histocompatibility class I antigen expressed on keratinocytes only during a neonatal period and not during adulthood. Blockade of T-cell migration neonatally prevented tolerance induction. The neonatally induced tolerance is maintained during adulthood, apparantly by a dominant regulatory mechanism. Thus, parenchymal cells and T-cell migration in the neonate contribute to the control of autoreactive T cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-065X.1999.tb01320.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Autoaggression and tumor rejection: it takes more than self-specific T-cell activation (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 169 (1999), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Establishment of self-tolerance prevents autoaggression against organ-specific self-antigens. This beneficial effect, however, may In turn be responsible for tumor immune evasion. Thus, dissecting the mechanisms leading to the breakdown of self-tolerance in autoimmune diseases might provide insights for successful antitumor immune therapies. In a variety of animal models, organ- or tumor-specific immunity has been described, focusing on antigen-specific T-cell activation. Here, we discuss two trans -genic mouse models which demonstrate that both autoaggression and tumor rejection require more than activated, self-reactive T cells. TCR transgenic mice, which are tolerant to a liver-specific MHC class I antigen, Kb, can be activated to reject Kbb-positive grafts, but fail to attack Kb-expressing liver. However, autoaggression occurs when activated T cells are combined with “conditioning” of the target organ by irradiation or infection with a liver-specific pathogen. Similarly, in a mouse model of islet cell carcinoma, neither co-stimulatory tumor cells nor highly activated antitumor lymphocytes provoke an effective immune response against the tumor. Instead, a combination of activated lymphocytes and irradiation is required for lymphocyte infiltration into solid tumors. Both model systems provide evidence that although activated antigen-specific lymphocytes are a prerequisite for autoaggression, effector cell extravasation and appropriate interaction with the target organ/tumor are equally important. Thus, we propose that the organ/tumor microenvironment is a critical parameter in determining the effectiveness of an anti-self immune response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-065X.1999.tb01321.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Inhibitors of animal phospholipase A2 enzymes are selective inhibitors of auxin-dependent growth. Implications for auxin-induced signal transduction (1997)
    Springer
    Planta 202 (1997), S. 462-469 
    Details
    ISSN: 1432-2048
    Keywords: Key words: Auxin ; Auxin inhibitor ; Cucurbita ; Elongation growth ; Phospholipase A inhibitor ; Signal transduction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract. Auxin and elicitors reportedly activate phospolipase A. A number of inhibitors known to inhibit animal phospholipase A2 were tested for their ability to inhibit hormone and fusicoccin-induced growth. To this end, growth induced by indolyl-3-acetic acid and 2,4-dichlorophenoxyacetic acid in hypocotyl segments of etiolated zucchini (Cucurbita pepo L.) seedlings was determined in the presence of the inhibitors nordihydroguajaretic acid (NDGA), aristolochic acid, 5,8,11,14-eicosatetraynoic acid (ETYA), PBx (a prostaglandin derivative), and oleylethyl phosphocholine. Each chemical proved inhibitory to auxin-induced growth, oleylethyl phosphocholine being the least effective. The effects of the first three inhibitors were investigated in more detail. Growth induced by 10 μM 2,4-dichlorophenoxyacetic acid or 1 μM indolyl-3-acetic acid was inhibited 50% by about 30–50 μM NDGA, by about 25 μM aristolochic acid, and by about 10–20 μM EYTA. Growth inhibition was reversible and became apparent 0.5–1 h after inhibitor addition. Growth induced by 0.5 or 1 μM fusicoccin was much less inhibited by NDGA and by ETYA, whereas aristolochic acid was only slightly less effective on fusicoccin-induced than on auxin-induced growth. These three inhibitors were also tested for their effects on gibberellin-induced growth in light-grown peas (Pisum sativum L.) and on cytokinin-induced expansion growth in excised cotyledons from radish (Raphanus sativum L.) seedlings. In both tests, aristolochic acid had toxic side-effects although gibberellin-induced growth was still apparent. In the gibberellin test, neither NDGA at up to 100 μM nor ETYA at 80 μM was inhibitory to hormone-induced growth. Moreover, 40 μM ETYA was not inhibitory to kinetin-induced growth. We hypothesize that the selectivity of phospholipase A2 inhibitors for auxin-induced growth implies a different signal transduction pathway for each of the different signal substances tested, and that auxins might use fatty acid(s) and/or lysophospholipid(s) or their derivatives as the preferred second messengers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004250050150
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...