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  • 1
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    Activation of interferon-gamma inducing factor mediated by interleukin-1beta converting enzyme (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: The interleukin-1beta (IL-1beta) converting enzyme (ICE) processes the inactive IL-1beta precursor to the proinflammatory cytokine. ICE was also shown to cleave the precursor of interferon-gamma inducing factor (IGIF) at the authentic processing site with high efficiency, thereby activating IGIF and facilitating its export. Lipopolysaccharide-activated ICE-deficient (ICE-/-) Kupffer cells synthesized the IGIF precursor but failed to process it into the active form. Interferon-gamma and IGIF were diminished in the sera of ICE-/- mice exposed to Propionibacterium acnes and lipopolysaccharide. The lack of multiple proinflammatory cytokines in ICE-/- mice may account for their protection from septic shock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gu, Y -- Kuida, K -- Tsutsui, H -- Ku, G -- Hsiao, K -- Fleming, M A -- Hayashi, N -- Higashino, K -- Okamura, H -- Nakanishi, K -- Kurimoto, M -- Tanimoto, T -- Flavell, R A -- Sato, V -- Harding, M W -- Livingston, D J -- Su, M S -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):206-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vertex Pharmaceuticals, Inc., 130 Waverly Street, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Caspase 1 ; Caspase 3 ; *Caspases ; Caspases, Initiator ; Culture Media, Conditioned ; Cysteine Endopeptidases/*metabolism ; Cytokines/blood/*metabolism/pharmacology ; Humans ; Interferon-gamma/biosynthesis/blood ; Interleukin-18 ; Kupffer Cells/*metabolism ; Lipopolysaccharides/pharmacology ; Mice ; Protein Precursors/metabolism ; Protein Processing, Post-Translational ; Recombinant Proteins/metabolism/pharmacology ; Spleen/cytology/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
    Electronic Resource
    Electronic Resource
    Induction of apoptosis in proliferating lymphocytes by tricyclic antidepressants (1998)
    Springer
    Apoptosis 3 (1998), S. 255-260 
    Details
    ISSN: 1573-675X
    Keywords: Antidepressants ; apoptosis ; induction ; lymphoblasts ; lymphocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We have previously found that tricyclic antidepressants (TCAs) induce apoptosis in quiescent human lymphocytes. The aim of the present study was to evaluate if TCAs induce apoptosis in proliferating human lymphocytes and in established blastoid lymphocytes also. The development of conA-induced lymphoblast populations was followed by measuring the CD25 membrane expression. Three TCA compounds were run with the following concentrations: imipramine (10, 20, 30, 40, 60μ M), clomipramine (1, 10, 20, 30, 40μ M) and citalopram (40, 60, 80, 100, 180μ M). They all induced a dose-dependent apoptosis both in continuously transformed, as well as in established lymphoblasts. Preincubation of the TCA up to 48 h did not significantly increase induction of apoptosis. The three drugs tested were found to be potent inducers of apoptosis in proliferating lymphocytes. Furthermore, we found that the apoptotic populations in proliferating and in established blastoid lymphocytes were of f airly the same magnitude than in the corresponding population in TCA-incubated resting lymphocytes. In conclusion, we demonstrate that TCAs induce apoptosis in proliferating lymphocytes, as they do in quiescent lymphocytes. Furthermore, the exent of apoptosis was even more pronounced in TCA-incubated lymphoblasts compared to TCA-treated resting lymphocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009609224936
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