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See detailCyclo-oxygenase type 2-dependent prostaglandin E-2 secretion is involved in retrovirus-induced T-cell dysfunction in mice
Rahmouni, Souad ULg; Aandahl, Einar Martin; Nayjib, Btissam ULg et al

in Biochemical Journal (2004), 384(Pt 3), 469-476

MAIDS (murine AIDS) is caused by infection with the murine leukaemia retrovirus RadLV-Rs and is characterized by a severe immunodeficiency and T-cell anergy combined with a lymphoproliferative disease ... [more ▼]

MAIDS (murine AIDS) is caused by infection with the murine leukaemia retrovirus RadLV-Rs and is characterized by a severe immunodeficiency and T-cell anergy combined with a lymphoproliferative disease affecting both B- and T-cells. Hyperactivation of the cAMP-protein kinase A pathway is involved in the T-cell dysfunction of MAIDS and HIV by inhibiting T-cell activation through the T-cell receptor. In the present study, we show that MAIDS involves a strong and selective up-regulation of cyclo-oxygenase type 2 in the CD11b+ subpopulation of T- and B-cells of the lymph nodes, leading to increased levels of PGE2 (prostaglandin E2). PGE2 activates the cAMP pathway through G-protein-coupled receptors. Treatment with cyclo-oxygenase type 2 inhibitors reduces the level of PGE2 and thereby reverses the T-cell anergy, restores the T-cell immune function and ameliorates the lymphoproliferative disease. [less ▲]

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See detailUSE OF COX-2 INHIBITORS FOR PREVENTING IMMUNODEFICIENCY
TASKÉN, Kjetil; Moutschen, Michel ULg; Rahmouni, Souad ULg et al

Patent (2002)

The present invention provides a method for treating or preventing a disorder typified by an immunodificiency (e.g. HIV), wherein the patient is administered a COX-2 inhibitor or derivative or ... [more ▼]

The present invention provides a method for treating or preventing a disorder typified by an immunodificiency (e.g. HIV), wherein the patient is administered a COX-2 inhibitor or derivative or pharmaceutically acceptable salt thereof, preferably diisopropylfluorophasphaate, L-745337, rofecoxi, NS 398, SC 58125, etodolac, meloxicam, celecoxib flusolide or nimesulide, and compositions and products containing the same or use of the same in preparing medicaments and for treatment. [less ▲]

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See detailIncreased Camp Levels and Protein Kinase (Pka) Type I Activation in Cd4+ T Cells and B Cells Contribute to Retrovirus-Induced Immunodeficiency of Mice (Maids): A Useful in Vivo Model for Drug Testing
Rahmouni, Souad ULg; Aandahl, Einar Martin; Trebak, Mohamed et al

in FASEB Journal (2001), 15(8), 1466-1468

Murine AIDS (MAIDS) is characterized by a lymphoproliferative disease and a profound anergy, which involves mostly CD4(+) T cells. To better define the mechanisms responsible for anergy, we measured cAMP ... [more ▼]

Murine AIDS (MAIDS) is characterized by a lymphoproliferative disease and a profound anergy, which involves mostly CD4(+) T cells. To better define the mechanisms responsible for anergy, we measured cAMP concentrations in the different lymphocyte subsets of the infected mice. CD4(+) T cells and B cells displayed a dramatic 10- to 30-fold increase of cAMP. cAMP was also significantly increased in CD8(+) T cells, although to a far lesser extent. The unusual CD4(+) CD90(-) T cells, typical of MAIDS, were characterized by a much higher cAMP level than their CD90(+) counterparts. T cells of the infected mice were much more sensitive to inhibition by the cAMP analogue 8-CPT-cAMP, which confirmed increased in vivo exposure to cAMP. In accordance with the increased cAMP levels, PKA type I was constitutively activated and its C subunit was translocated to the nucleus. Finally, the profound T-cell anergy associated with MAIDS could be reversed by treating T cells with a PKA type I-selective antagonist ex vivo. MAIDS could constitute a suitable model for the study of new pharmacological agents aimed at reversing the immunosuppressive effects of cAMP previously shown to be involved in several pathological states, including HIV infection and common variable immunodeficiency. [less ▲]

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