Fibroblast-derived factors preserve viability in vitro of mononuclear cells isolated from subjects with HIV-1 infection

CD8+ lymphocyte phenotype and cytokine production in long-term non-progressor and in progressor patients with HIV-1 infection

“…Also the study of cytokine production profiles can be used for this purpose: a switch from Th1 to Th2 cytokine-producing cells in the course of the disease has been suggested to be associated with deteriorating immunological functions [9,19]. Previous studies have also shown that CD28 and IL-2 production are reduced in HIV infection, and that in HIV , but p24-negative subjects, IL-2 is a key factor of the immunological response, because of its ability to reduce the mortality of CD8 CD28 non-activated cells [20][21][22]. The groups studied, however, are composed of a heterogeneous population, including also recent seroconverters and progressors, while LTNP have never been investigated as a separate and distinct entity; they represent, in fact, a selected group of patients differing from most HIV-infected subjects for their peculiar clinical and immunological aspects.…”

Low-Dose IL-2 Reduces Lymphocyte Apoptosis and Increases Naive CD4 Cells in HIV-1 Patients Treated with HAART

“…Increased in vitro spontaneous apoptosis has been consistently observed in peripheral blood mononuclear cells (PBMC) of human immunodeficiency virus type 1 (HIV-1)-infected patients (1)(2)(3). We have previously shown that the rate of apoptosis correlates with disease severity and progression (4).…”

“…It has been hypothesized that, during HIV infection, increased numbers of activated CD8 cells (11,12) undergo apoptosis because the rescue mechanisms provided by activation-supporting cytokines such as interleukin (IL)-2 are not sufficiently produced by impaired CD4 ϩ T cells (13). Several studies have shown that apoptosis can be diminished by the addition of IL-2 (3,14,15) to the lymphocyte cultures.…”

Immune dysregulation and CD4+ T cell loss in HIV-1 infection

“…Our finding that, in vitro, growth factors could not prevent the death of cells from HIV-infected individuals, does not exclude such a mechanism but may indicate that cells from HIV-infected individuals are already irreversibly primed for PCD in vivo [95]. Other groups, however, have reported rescue of cells from HIV-infected individuals from apoptosis by combinations of growth factors [59,61,121]. Furthermore, apoptosis has been reported to be differentially influenced by Thl and Th2 cytokines.…”

“…Ameisen and Capron [3] were the first to propose that in HIV infection interaction of soluble gp 120 with CD4, previously shown to lead to impaired lymphocyte function [26], could prime CD4 + T cells for PCD, which might provide a mechanism for CD4 + T cell loss. Indeed, peripheral blood mononuclear cells (PBMC) from HIV-infected individuals die due to PCD in vitro [59,61,78,94,95,117,121]. PCD can be enhanced by activation in vitro with T cell receptor (TCR)/CD3 monoclonal antibodies (mAb), lectins, superantigens or ionomycin [59,61,94,117].…”