Downregulation of Increased CD95 (APO-1/Fas) Ligand in T Cells From Human Immunodeficiency Virus-Type 1–Infected Children After Antiretroviral Therapy

Böhler, Thomas; Herr, Ingrid; Debatin, Klaus‐Michael; Geiss, Magdalena; Haas, Jürgen

doi:10.1182/blood.v90.2.886.886_886_887

Cited by 8 publications

(3 citation statements)

References 6 publications

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“…Although the evidence for a direct correlation between the level of viral load and cell apoptosis is still questionable [45], results on the use of highly active anti-retroviral therapy suggest a direct relationship between sustained suppression of viral replication and enhanced lymphocyte count or immune recovery [46]. Moreover, effective anti-retroviral treatment has been recently demonstrated to result in down-regulation of CD95-ligand expression on T cells, suggesting that significant reduction in virus replication could lead to a decrease in the PCD of uninfected cells [47]. Thus, therapeutics capable of inhibiting viral replication and simultaneously blocking AICD may have stronger and more rapid effects in the treatment of HIV disease.…”

Section: Discussionmentioning

confidence: 99%

Recombinant human IL-16 inhibits HIV-1 replication and protects against activation-induced cell death (AICD)

Idziorek

Khalife

Billaut-Mulot

et al. 1998

Clinical and Experimental Immunology

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The chemoattractant cytokine IL- 16 has been reported to suppress lymphocyte activation and to inhibit HIV-1 replication in acutely infected T cells. We have cloned and expressed human IL-16 in Escherichia coli and investigated whether the recombinant protein could regulate the level of lymphocyte apoptosis from HIV-1-infected subjects. After purification and refolding, only 2-10% of the recombinant cytokine was present in a biologically active homotetrameric form. This could explain the need for high concentrations of the bacterially derived IL- 16 to induce significant inhibition of HIV-1 replication. Addition of IL-16 to unstimulated peripheral blood mononuclear cell (PBMC) cultures from HIV-1-infected subjects did not modify the observed level of spontaneous lymphocyte apoptosis. In contrast, IL-16 added to PBMC cultures stimulated with anti-CD3, anti-CD95 or dexamethasone reduced significantly the percentage of lymphocytes undergoing AICD. This effect was found to correlate with the ability of the cytokine to decrease CD95 expression on activated CD4+ T cells. Comparative studies on PBMC from healthy individuals indicated that the regulation of apoptosis levels by IL-16 is a complex phenomenon and could depend on the nature of the activator used and/or the immune status of lymphocytes tested. The outcome of CD4 cross-linking on T cells by various ligands is discussed in the context of the observed beneficial activities of IL- 16 and its potential role in the treatment of HIV disease.

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Section: Discussionmentioning

confidence: 99%

Recombinant human IL-16 inhibits HIV-1 replication and protects against activation-induced cell death (AICD)

Idziorek

Khalife

Billaut-Mulot

et al. 1998

Clinical and Experimental Immunology

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“…Persistent HIV viremia has also been related to an increase in T cell apoptosis. A higher expression of the key regulatory marker of apoptosis (CD95) on CD4 + has been described during HIV infection [ 24 – 26 ]. Conversely, a significant decrease in CD95 expression, with the reduction of CD4 + and CD8 + T cells apoptosis, has been observed after HAART initiation in HIV-infected children and adolescents [ 27 ].…”

Section: Factors Leading To Suboptimal Reconstitution Of T-cell Comentioning

confidence: 99%

Suboptimal Immune Reconstitution in Vertically HIV Infected Children: A View on How HIV Replication and Timing of HAART Initiation Can Impact on T and B-cell Compartment

Cotugno

Douagi

Rossi

et al. 2012

Clinical and Developmental Immunology

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Today, HIV-infected children who have access to treatment face a chronic rather than a progressive and fatal disease. As a result, new challenges are emerging in the field. Recent lines of evidence outline several factors that can differently affect the ability of the immune system to fully reconstitute and to mount specific immune responses in children receiving HAART. In this paper, we review the underlying mechanisms of immune reconstitution after HAART initiation among vertically HIV-infected children analyzing the possible causes of suboptimal responses.

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“…Η αλληλεπίδραση των αυξηµένων ποσοτήτων FasL µε τον επιφανειακό υποδοχέα Fas φαίνεται να είναι η κύρια αιτία θανάτου των PBMC από µολυσµένους ασθενείς in vitro, καθώς η αναστολή αυτής της αλληλεπίδρασης µε διαλυτό Fas ή κατάλληλα ανταγωνιστικά anti-Fas αντισώµατα εµποδίζει την ex vivo απόπτωση των παραπάνω κυττάρων (Dockrell et al, 1999). Τα επίπεδα έκφρασης του FasL στα PBMC φορέων και η επακόλουθη απώλεια των CD4+ κυττάρων µειώνονται επίσης µετά τη χορήγηση αντιρετροικής θεραπείας, κάτι που δεν συµβαίνει όµως στα κύτταρα των λεµφικών οργάνων (Bohler et al, 1997).…”

Section: 23α μέτρηση ιοντικών αλληλεπιδράσεων µε τη µέθοδο Sprunclassified

Μελέτη των μηχανισμών απορρύθμισης της λειτουργίας των ανοσοδραστικών CD4+T κυττάρων από τη V3 περιοχή της γλυκοπρωτεΐνης gp120 του ιού HIV-1

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Downregulation of Increased CD95 (APO-1/Fas) Ligand in T Cells From Human Immunodeficiency Virus-Type 1–Infected Children After Antiretroviral Therapy

Cited by 8 publications

References 6 publications

Recombinant human IL-16 inhibits HIV-1 replication and protects against activation-induced cell death (AICD)

Recombinant human IL-16 inhibits HIV-1 replication and protects against activation-induced cell death (AICD)

Suboptimal Immune Reconstitution in Vertically HIV Infected Children: A View on How HIV Replication and Timing of HAART Initiation Can Impact on T and B-cell Compartment

Μελέτη των μηχανισμών απορρύθμισης της λειτουργίας των ανοσοδραστικών CD4+T κυττάρων από τη V3 περιοχή της γλυκοπρωτεΐνης gp120 του ιού HIV-1

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