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13 results on '"Jaleco, Sara"'

4. Release of IL-1β via IL-1β-Converting Enzyme in a Skin Dendritic Cell Line Exposed to 2,4-Dinitrofluorobenzene

Author

Matos, Teresa J., Jaleco, Sara P., Gonçalo, Margarida, Duarte, Carlos B., and Lopes, M. Celeste

Subjects
Caspase 1, Receptors, Interleukin-1, Dendritic Cells, Cysteine Proteinase Inhibitors, Caspase Inhibitors, Amino Acid Chloromethyl Ketones, Cell Line, Research Communication, Mice, lcsh:Pathology, Animals, Dinitrofluorobenzene, Protein Processing, Post-Translational, Interleukin-1, Skin, lcsh:RB1-214
Abstract

We used a mouse fetal skin dendritic cell line (FSDC) to study the effect of the strong allergen 2,4-dinitrofluorobenzene (DNFB) on interleukin (IL)-1beta release and IL-1beta receptor immunoreactivity. Stimulation with DNFB (30 minutes) increased IL-1 release without changing the mRNA levels of the protein. Furthermore, DNFB increased transiently the interleukin-1beta-converting enzyme (ICE) activity, as measured with its fluorogenic substrate Z-Tyr-Val-Ala-Asp-AFC. The ICE inhibitor Z-YVAD-FMK prevented the release of IL-1beta evoked by DNFB. Incubation of the cells with DNFB (30 minutes) strongly increased IL-1beta receptor immunoreactivity. The rapid effect of DNFB on the release of mature IL-1beta, without inducing an increase of IL-1beta mRNA in FSDC, suggests a posttranslational modification of pro-IL-1beta by ICE activity.

Published
2005

5. IL-7 differentially regulates cell cycle progression and HIV-1-based vector infection in neonatal and adult [CD4.sup.+] T cells

Author

Dardalhon, Valerie, Jaleco, Sara, Kinet, Sandrina, Herpers, Bjorn, Steinberg, Marcos, Ferrand, Christophe, Froger, Delphine, Leveau, Christelle, Tiberghien, Pierre, Charneau, Pierre, Noraz, Nelly, and Taylor, Naomi

Subjects
HIV infection -- Research, T cells -- Research, Science and technology
Abstract

Differences in the immunological reactivity of umbilical cord (UC) and adult peripheral blood (APB) T cells are poorly understood. Here, we show that IL-7, a cytokine involved in lymphoid homeostasis, has distinct regulatory effects on APB and UC lymphocytes. Neither naive nor memory APB [CD4.sup.+] cells proliferated in response to IL-7, whereas naive UC [CD4.sup.+] lymphocytes underwent multiple divisions. Nevertheless, both naive and memory IL-7-treated APB T cells progressed into the [G.sub.1b] phase of the cell cycle, albeit at higher levels in the latter subset. The IL-7-treated memory [CD4.sup.+] lymphocyte population was significantly more susceptible to infection with an HIV-1-derived vector than dividing [CD4.sup.+] UC lymphocytes. However, activation through the T cell receptor rendered UC lymphocytes fully susceptible to HIV-1-based vector infection. These data unveil differences between UC and APB [CD4.sup.+] T cells with regard to IL-7-mediated cell cycle progression and HIV-1-based vector infectivity. This evidence indicates that IL-7 differentially regulates lymphoid homeostasis in adults and neonates.

Published
2001

9. IL-7 and CD4+ T-cell proliferation

Author

Jaleco, Sara, primary, Kinet, Sandrina, additional, Hassan, Jaythoon, additional, Dardalhon, Valérie, additional, Swainson, Louise, additional, Reen, Denis, additional, and Taylor, Naomi, additional

Published
2002
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11. IL-7 differentially regulates cell cycle progression and HIV-1-based vector infection in neonatal and adult CD4+T cells

Author

Dardalhon, Valérie, primary, Jaleco, Sara, additional, Kinet, Sandrina, additional, Herpers, Bjorn, additional, Steinberg, Marcos, additional, Ferrand, Christophe, additional, Froger, Delphine, additional, Leveau, Christelle, additional, Tiberghien, Pierre, additional, Charneau, Pierre, additional, Noraz, Nelly, additional, and Taylor, Naomi, additional

Published
2001
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12. Binding of Human Immunodeficiency Virus Type 1 gp120 to CXCR4 Induces Mitochondrial Transmembrane Depolarization and Cytochromec-Mediated Apoptosis Independently of Fas Signaling

Author

Roggero, Rodolphe, Robert-Hebmann, Ve´ronique, Harrington, Steve, Roland, Joachim, Vergne, Laurence, Jaleco, Sara, Devaux, Christian, and Biard-Piechaczyk, Martine

Abstract

ABSTRACTApoptosis of CD4+T lymphocytes, induced by contact between human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein (gp120) and its receptors, could contribute to the cell depletion observed in HIV-infected individuals. CXCR4 appears to play an important role in gp120-induced cell death, but the mechanisms involved in this apoptotic process remain poorly understood. To get insight into the signal transduction pathways connecting CXCR4 to apoptosis following gp120 binding, we used different cell lines expressing wild-type CXCR4 and a truncated form of CD4 that binds gp120 but lacks the ability to transduce signals. The present study demonstrates that (i) the interaction of cell-associated gp120 with CXCR4-expressing target cells triggers a rapid dissipation of the mitochondrial transmembrane potential resulting in the cytosolic release of cytochrome cfrom the mitochondria to cytosol, concurrent with activation of caspase-9 and -3; (ii) this apoptotic process is independent of Fas signaling; and (iii) cooperation with a CD4 signal is not required. In addition, following coculture with cells expressing gp120, a Fas-independent apoptosis involving mitochondria and caspase activation is also observed in primary umbilical cord blood CD4+T lymphocytes expressing high levels of CXCR4. Thus, this gp120-mediated apoptotic pathway may contribute to CD4+T-cell depletion in AIDS.

Published
2001
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