scholarly journals Production of and in vitro response to interleukin 2 in the acquired immunodeficiency syndrome.

1985 ◽  
Vol 76 (5) ◽  
pp. 1959-1964 ◽  
Author(s):  
H W Murray ◽  
K Welte ◽  
J L Jacobs ◽  
B Y Rubin ◽  
R Mertelsmann ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Interleukin 2 ◽  
In Vitro Response ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

Intralymphatic Interleukin 2 Treatment in Patients with Acquired Immunodeficiency Syndrome: Preliminary Experience in Three Cases

Immunobiology ◽  
1986 ◽  
Vol 172 (3-5) ◽  
pp. 438-447 ◽  
Author(s):  
M. Gramatzki ◽  
H. Nüsslein ◽  
G.R. Burmester ◽  
W. Rüdl ◽  
N. Heyder ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Interleukin 2 ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

scholarly journals CD4 T cells in murine acquired immunodeficiency syndrome: polyclonal progression to anergy.

1992 ◽  
Vol 175 (6) ◽  
pp. 1589-1599 ◽  
Author(s):  
G Muralidhar ◽  
S Koch ◽  
M Haas ◽  
S L Swain
Keyword(s):  
T Cells ◽  
T Cell ◽  
Acquired Immunodeficiency Syndrome ◽  
Cd4 T Cells ◽  
Interleukin 2 ◽  
Cell Subset ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Phenotypic Shift ◽  
Kinetics Of

We have examined the kinetics of changes that occur in the helper T cell subset during murine acquired immunodeficiency syndrome, which occurs after infection with the mix of viruses known as BM5. We find that there is expansion of the CD4 T cells by 2 wk, 50% of the CD4 T cells become large as the disease progresses, and the CD4 T cell population is increasingly comprised of cells with a memory/activated phenotype. These effects are apparent by 2 wk postinfection, and the change is nearly complete by 6-8 wk. The phenotypic shift is paralleled by the loss of the ability of the CD4 T cells to proliferate or to produce interleukin 2 (IL-2), IL-3, IL-4, and interferon gamma in response to stimulation with mitogens, superantigen, or anti-CD3. There is no obvious expansion or deletion of CD4 T cells expressing particular V beta genes, as might be expected if a conventional superantigen were driving the changes. The results suggest, however, that the total CD4 population has been driven to anergy by some potent polyclonal stimulus directly associated with viral infection.

Rapid Death of Adoptively Transferred T Cells in Acquired Immunodeficiency Syndrome

Blood ◽  
1999 ◽  
Vol 93 (5) ◽  
pp. 1506-1510 ◽  
Author(s):  
Rusung Tan ◽  
Xiaoning Xu ◽  
Graham S. Ogg ◽  
Pokrath Hansasuta ◽  
Tao Dong ◽  
...  
Keyword(s):  
T Cell ◽  
Adoptive Transfer ◽  
Acquired Immunodeficiency Syndrome ◽  
Mononuclear Cells ◽  
Virus Load ◽  
Acquired Immunodeficiency ◽  
Peptide Complexes ◽  
Immunodeficiency Syndrome

Human immunodeficiency virus (HIV)-specific cytotoxic T lymphocytes (CTL) probably play the major role in controlling HIV replication. However, the value of adoptive transfer of HIV-specific CTL expanded in vitro to HIV+ patients has been limited: this contrasts with the success of CTL therapy in treating or preventing Epstein-Barr virus and cytomegalovirus disease after bone marrow transplantation (BMT). We investigated the fate of expanded HIV-specific CTL clones in vivo following adoptive transfer to a patient with acquired immunodeficiency syndrome (AIDS). Two autologous CTL clones specific for HIV Gag and Pol were expanded to large numbers (>109) in vitro and infused into an HIV-infected patient whose viral load was rising despite antiretroviral therapy. The fate of one clone was monitored by staining peripheral blood mononuclear cells (PBMCs) with T-cell receptor–specific tetrameric major histocompatibility complex (MHC)-peptide complexes. Although the CTL transfer was well tolerated, there were no significant changes in CD4 and CD8 lymphocyte counts and virus load. By tracking an infused clone using soluble MHC-peptide complexes, we show that cells bearing the Gag-specific T-cell receptors were rapidly eliminated within hours of infusion through apoptosis. Thus, the failure of adoptively transferred HIV-specific CTL to reduce virus load in AIDS may be due to rapid apoptosis of the infused cells, triggered by a number of potential mechanisms. Further trials of adoptive transfer of CTL should take into account the susceptibility of infused cells to in vivo apoptosis.

Activation of monocyte-mediated tumoricidal activity in patients with acquired immunodeficiency syndrome.

1985 ◽  
Vol 3 (7) ◽  
pp. 1005-1012 ◽  
Author(s):  
E S Kleinerman ◽  
L M Ceccorulli ◽  
L A Zwelling ◽  
T Twilley ◽  
R B Herberman ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Mononuclear Cells ◽  
Human Tumor ◽  
Target Cells ◽  
Aids Patients ◽  
Tumoricidal Activity ◽  
Ifn Gamma ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

The purpose of these studies was to determine whether peripheral blood monocytes from acquired immunodeficiency syndrome (AIDS) patients with Kaposi's sarcoma could be activated to lyse human tumor target cells in vitro. Monocytes were isolated and incubated for 24 hours in vitro with either medium (control), a crude mitogen-induced lymphokine preparation (MAF), or endotoxin before the addition of [125I]IUdR-labeled A375 melanoma target cells. Cytolysis was determined 72 hours later. Twelve (100%) of 12 patients tested had monocyte-mediated cytotoxicity values that were comparable to those of normal individuals. Recombinant human gamma interferon (IFN gamma) activated both normal and AIDS monocyte-mediated tumoricidal function only when combined with lypopolysaccharide (LPS). In addition, mononuclear cells from ten AIDS patients were also tested for their ability to secrete MAF and IFN gamma in response to a mitogenic stimulus. Lymphokines generated from all ten patients contained substantial amounts of IFN gamma (100 to 2,500 U/mL); however, three of these ten lymphokine preparations failed to activate normal monocytes to lyse tumor cells. These results suggest that monocyte-mediated tumoricidal function of AIDS patients is intact and thus suggest new approaches for the therapy of AIDS.

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