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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 19-26 
    ISSN: 1432-1440
    Keywords: Hodgkin's disease ; Autologous mixed leukocyte culture test ; Cellular immunity ; Immunosuppression ; Morbus Hodgkin ; autologe gemischte Lymphozytenkultur ; zelluläre Immunität ; Immunsuppression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die gestörte Funktion des Immunsystems, besonders die der zellulären Immunabwehr ist bei Patienten mit Morbus Hodgkin seit langem bekannt. Dabei steht der verminderten Reaktivität der peripheren Blutlymphozyten eine gesteigerte Lymphozytopoese in lymphatischen Organen mit Hyperplasie dieser Gewebe gegenüber. Wir untersuchten die Reaktivität peripherer T-Lymphozyten von 20 Patienten mit Morbus Hodgkin und 26 gesunden Kontrollpersonen gegen autologe und allogene Nicht-T-Lymphozyten in der gemischten Lymphozytenkultur (MLC). Unsere Versuche hatten folgende Ergebnisse: (1) T-Lymphozyten von Morbus Hodgkin-Patienten werden nicht oder nur sehr schwach in der autologen MLC stimuliert. (2) In der allogenen MLC reagieren T-Zellen von Patienten deutlich stärker als in der autologen MLC, jedoch significant geringer als normale T-Lymphozyten gegen normale Nicht-T-Lymphozyten. Nicht-T-Zellen von Patienten stimulieren dagegen allogene T-Lymphozyten von Gesunden kaum weniger als normale Nicht-T-Zellen. (3) Wird eine autologe MLC mit Lymphozyten gesunder Spender, jedoch mit Serum von Patienten mit Morbus Hodgkin durchgeführt, zeigt sich eine signifikante, dosisabhängige Verminderung der Reaktivität gegenüber Kontrollen mit Serum von Normalpersonen. Diese Ergebnisse zeigen zusammengefaßt bei Patienten mit Morbus Hodgkin eine gestörte Funktion der T-Lymphozyten in der autologen MLC und die Existenz eines oder mehrerer Serumfaktoren, die die Proliferation von T-Lymphozyten gesunder Personen in der autologen MLC hemmen. Die Rolle von Suppressorzellen und derer Faktoren als Ursache für diese Befunde wird diskutiert.
    Notes: Summary In patients with Hodkin's disease, the impaired immune reactivity, especially of the thymus dependent system, is well established. This decreased immune response of the lymphocytes from the peripheral blood contrasts to an increased lymphocytopoiesis in the lymphatic organs with a hyperplasia of these tissues. We studied the reactivity of peripheral T lymphocytes from 20 patients with Hodgkin's disease and 26 healthy control persons against autologous and allogeneic non T cells respectively in the mixed lymphocyte culture (MLC). Our experiments show an extremely depressed autologous mixed lymphocyte reactivity (MLR) of T lymphocytes from patients with Hodgkin's disease compared to those from normal donors. In the allogeneic MLC, the proliferation of the patients' T cells was stronger than in the autologous MLC, but significantly lower than the proliferation of normal T lymphocytes when stimulated by normal non T cells. Patients' non T cells stimulated T lymphocytes from healthy donors as well as non T lymphocytes from normals did. Finally, the autologous MLR of normal lymphocytes was significantly suppressed by 18 of 23 sera from Hodgkin's patients when these sera were substituted for normal AB serum in the cultures. These results demonstrate an impaired function of T lymphocytes from patients with Hodgkin's disease in the autologous MLC and the presence of one or more factors in their serum which inhibit the proliferation of normal lymphocytes in the autologous MLC. The role of suppressor cells and their factors will be discussed.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Nuclear Instruments and Methods In Physics Research 201 (1982), S. 287-290 
    ISSN: 0167-5087
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Physics
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-675X
    Keywords: Apoptosis ; cyclin D1 ; growth inhibition ; senescence.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract It is now apparent that apoptosis is closely linked to the control of cell cycle progression. During the G1 to S progression, cyclin D1, p53, and the cyclin dependent kinase inhibitors p21WAF1 and p27kip1 can play roles in induction of apoptosis. During the G2 and M phases, premature activation of Cdk1 can cause cells to enter mitotic catastrophe, which results in apoptosis. In this review we focus on factors acting during G1 and S, particularly cyclin D1, and their effects on cell growth, senescence and apoptosis. We emphasize that cyclin D1 can have diverse effects on cells depending on its level of expression, the specific cell type, the cell context and other factors. Possible mechanisms by which cyclin D1 exerts these diverse effects, via cyclin dependent kinase-dependent and -independent pathways, are discussed.
    Type of Medium: Electronic Resource
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