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  • 1
    ISSN: 1573-4919
    Keywords: T-cell receptor (TCR) ; TCRζ gene locus ; dexamethasone ; glucocorticoids ; splicing
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract T-cell receptor (TCR) is a multichain receptor in which the TCRζ subunit is important for membrane assembly and signal transduction. Four alternative splicings of the murine TCRζ gene locus have been previously described. We here describe a new alternative splicing of murine TCRζ gene, TCRκ, cloned by RT-PCR, that is encoded by exons 1-7, a portion of exon 9 and the whole exon 10 of TCRζ gene. The protein encoded by TCRκ mRNA is identical to that encoded by TCRκ mRNA, because the stop codon is present in the exon 9 before splicing with exon 10. RNAse protection assays carried out on total RNA from thymocytes indicate that TCRκ mRNA is 1 half with respect to TCRκ mRNA, suggesting that TCRκ mRNA contributes to determine the TCRκ protein levels. The 3′ untranslated region of TCRκ mRNA is different from that of TCRκ and this might lead to different t1/2 for each species in vivo. We also show that dexamethasone (DEX), a synthetic glucocorticoid hormone, increases the amount of TCRκ in the hybridoma T-cell line 3DO (about 5-fold increase), as indicated by reverse transcriptase-polymerase chain reaction (RT-PCR) and RNAse protection assays. This newly described effect of DEX may constitute a further molecular mechanism that contributes to its immunomodulating activity.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The natural killer (NK) cell activity of DBA/2J mice infected with the polycythemic variant of Friend leukemia virus (FLV-P) declines early after virus challenge, being non-detectable 2 weeks after FLV-P inoculation. Cells capable of suppressing the in vitro cytolytic activity of NK effector lymphocytes were detected in the spleen of infected mice. The mechanism of suppression could be based on cell-mediated impairment of NK effector function, or on antigenic competition from splenocytes expressing NK antigens elicited by FLV-P.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 167 (1997), S. 135-144 
    ISSN: 1573-4919
    Keywords: glucocorticoid hormones ; T lymphocytes ; T-cell receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Glucocorticoid hormones (GCH) are anti-inflammatory and immunosuppressive agents that inhibit T-cell growth and activation. Since the T-cell receptor (TCR)/CD3 complex mediates T-lymphocyte activation, we studied the effect of in vitro dexamethasone (DEX), a synthetic GCH, on TCR/CD3 expression. DEX-treatment of a hybridoma T-cell line and normal un-transformed T-cell clones induced a decrease of the TCR/CD3 membrane expression after 4 days. After 4 weeks, TCR/CD3 was undetectable. However, the amount of mRNAs coding TCR/CD3 chains, including TCRα, TCRβ, CD3γ, CD3δ and CD3ε, as well as the amount of CD3ε protein, a major component of the complex, were unaltered. By contrast, a decrease of the mRNAs deriving from the TCRζ gene locus, as well as of the TCRζ protein which is responsible for the membrane expression of the TCR/CD3 complex, was induced. These data suggest that the down-modulation of TCR expression is due to the diminution of TCRζ gene products in DEX-treated cells. (Mol Cell Biochem 167: 135-144, 1997)
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-4919
    Keywords: phosphatidylserine ; base exchange ; apoptosis ; thymocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The exposure of phosphatidylserine toward the external surface of the membrane is a well-established event of programmed cell death. The possibility that an apoptotic stimulus influences the metabolism of this phospholipid could be relevant not only in relation to the previously mentioned event but also in relation to the capability of membrane phosphatidylserine to influence PKC activity. The present investigation demonstrates that treatment of mouse thymocytes with the apoptotic stimulus dexamethasone, enhances the incorporation of [3H]serine into phosphatidylserine. Cell treatment with dexamethasone also enhanced the activity of serine base exchange enzyme, assayed in thymocyte lysate. Both the effects were observed at periods of treatment preceding DNA fragmentation. The addition of unlabelled ethanolamine, together with [3H]serine to the medium containing dexamethasone-treated thymocytes lowered the radioactivity into phosphatidylserine. Serine base exchange enzyme activity was influenced by the procedure used to prepare thymocyte lysate and was lowered by the addition of fluoroaluminate, that is widely used as a G-protein activator. The increase of serine base exchange enzyme activity induced by dexamethasone treatment was observed independently by the procedure used to prepare cell lysate and by the presence or absence of fluoroaluminate.
    Type of Medium: Electronic Resource
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