A Longitudinal Study of a Patient with Acquired Immunodeficiency Syndrome Using T Cell Subset Analysis

1983 ◽  
pp. 295-303 ◽  
Author(s):  
R. Lawrence Siegel ◽  
Roger W. Fox
Keyword(s):  
Longitudinal Study ◽  
T Cell ◽  
Acquired Immunodeficiency Syndrome ◽  
Cell Subset ◽  
T Cell Subset ◽  
Subset Analysis ◽  
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.

Angiotropic (Intravascular) Large Cell Lymphoma of T-Cell Phenotype Presenting as Acute Appendicitis in a Patient With Acquired Immunodeficiency Syndrome

1999 ◽  
Vol 123 (4) ◽  
pp. 335-337 ◽  
Author(s):  
Denise M. Malicki ◽  
Yae K. Suh ◽  
Gregory N. Fuller ◽  
Sung S. Shin
Keyword(s):  
T Cell ◽  
Acute Appendicitis ◽  
Acquired Immunodeficiency Syndrome ◽  
Cell Lymphoma ◽  
Immunohistochemical Analysis ◽  
Large Cell ◽  
Cell Phenotype ◽  
Acquired Immunodeficiency ◽  
Large Cell Lymphoma ◽  
Immunodeficiency Syndrome

Abstract We describe a patient with acquired immunodeficiency syndrome who presented with acute appendicitis but was found to have angiotropic large cell lymphoma (ALCL) by pathologic examination of the appendectomy specimen, without acute inflammation. Very rare cases of angiotropic large cell lymphoma have been reported in patients with human immunodeficiency virus infection, and most cases of this rare lymphoma are of B-cell origin, but in this instance immunohistochemical analysis showed a T-cell phenotype.

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.

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