Syncytium Formation and Destruction of Bystander CD4+ Cells Cocultured with T Cells Persistently Infected with Human Immunodeficiency Virus as Demonstrated by Flow Cytometry

ABSTRACT An alternative technology for the estimation of T cells based on a microcapillary technique (Guava Technologies, Hayward, CA) was compared to FACSCount (Becton Dickinson, San Jose, CA). Samples from 51 human immunodeficiency virus-infected and 21 healthy individuals were tested. The correlation (r) of the two systems for CD4+ T cells was 0.994, and the coefficient of variation was 6.5%, establishing equable performance between the two technologies.

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Flow cytometry crossmatch reactivity with pronase-treated T cells induced by non-HLA autoantibodies in human immunodeficiency virus-infected patients

Human Immunology ◽

10.1016/j.humimm.2016.04.014 ◽

2016 ◽

Vol 77 (6) ◽

pp. 449-455 ◽

Cited By ~ 11

Author(s):

Katarzyna Szewczyk ◽

Kelly Barrios ◽

Daniel Magas ◽

Kristin Sieg ◽

Bozena Labuda ◽

...

Keyword(s):

Flow Cytometry ◽

Human Immunodeficiency Virus ◽

T Cells ◽

Immunodeficiency Virus

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CD8+ T lymphocytes provide helper activity for IgE synthesis in human immunodeficiency virus-infected patients with hyper-IgE.

Journal of Experimental Medicine ◽

10.1084/jem.181.1.423 ◽

1995 ◽

Vol 181 (1) ◽

pp. 423-428 ◽

Cited By ~ 66

Author(s):

R Paganelli ◽

E Scala ◽

I J Ansotegui ◽

C M Ausiello ◽

E Halapi ◽

...

Keyword(s):

Human Immunodeficiency Virus ◽

T Cells ◽

T Cell ◽

Hiv Infection ◽

Cd8 T Cells ◽

Cd8 T Cell ◽

Cd4 Cells ◽

In Vitro Synthesis ◽

Immunodeficiency Virus ◽

Ige Synthesis

Increased levels of serum IgE and eosinophilia have been described in human immunodeficiency virus (HIV) infection, almost exclusively in patients with CD4+ cell count < 200 cells/microliters. IgE production is regulated by CD4+ T helper type 2 (Th-2) lymphocytes, producing interleukin 4 (IL-4) and expressing a ligand for the B cell-specific CD40 molecule (CD40 ligand [L]). A shift to a Th-2-like pattern of cytokine secretion has been postulated to be associated with progression toward acquired immunodeficiency syndrome (AIDS). We studied three AIDS patients with very high levels of IgE and almost complete depletion of CD4+ lymphocytes, suggesting that IgE synthesis could not be driven by CD4+ cells. IgE in vitro synthesis by cells from such patients was, however, inhibited by anti-IL-4. We show that both CD8+ T cell lines and the majority of CD8+ T cells clones derived from these patients produce IL-4, IL-5, and IL-6 in half of the cases together with interferon gamma (IFN-gamma). 44% of CD8+ T cell clones expressed a CD40L, and the supernatants of the clones were capable of inducing IgE synthesis by normal B cells costimulated with anti-CD40. CD8+ T cells in these patients therefore functionally mimic Th-2 type cells and may account for hyper-IgE and eosinophilia in the absence of CD4+ cells. The presence of such CD8+ cells may also provide a source of IL-4 directing the development of predominant Th-2 responses in HIV infection.

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Gag-Specific CD8 T-Cell Proliferation Is Associated With Higher Peripheral Blood Levels of Transforming Growth Factor-β and Gut-Homing T Cells in Youths Perinatally Infected With Human Immunodeficiency Virus-1: The ANRS-EP38-IMMIP Study

Open Forum Infectious Diseases ◽

10.1093/ofid/ofw239 ◽

2016 ◽

Vol 4 (1) ◽

Author(s):

Josiane Warszawski ◽

Véronique Avettand-Fenoel ◽

Christine Rouzioux ◽

Daniel Scott-Algara ◽

Thomas Montange ◽

...

Keyword(s):

Flow Cytometry ◽

Human Immunodeficiency Virus ◽

Cell Proliferation ◽

T Cells ◽

T Cell ◽

Transforming Growth Factor ◽

Cd8 T Cell ◽

T Cell Proliferation ◽

Immunodeficiency Virus ◽

Tgf Β1

Abstract Background Gag-specific T lymphocytes play a key role in the control of human immunodeficiency virus (HIV) replication. Their restoration will be important for future reservoir targeting strategies. In this study, we aimed to identify immune correlates of Gag-specific CD8 T-cell proliferation in youths with perinatally acquired HIV-1 infection. Methods The ANRS-EP38-IMMIP study included youths of 15 to 24 years of age. Fifty-three were taking combination anti-retroviral therapy and aviremic at the time of the study and had undergone valid 5-6-carboxyfluorescein diacetate succimidyl ester-based flow cytometry T-cell proliferation assays. Plasma analytes were quantified by enzyme-linked immunosorbent assay or multiplex assays. Peripheral blood cells were phenotyped by flow cytometry. Logistic regression was used to study the association between Gag-specific T-cell proliferation and immune markers. Results Patients with Gag-specific CD8 T-cell proliferation had higher levels of plasma transforming growth factor (TGF)-β1, a lower proportion of naive cells among regulatory T cells (Tregs), and higher percentages of CD4 and CD8 T cells expressing the α4β7 integrin or CD161 molecule than those without a Gag-specific response. These associations were significant based on analyses including potential confounders. Conclusions Preserved Gag-specific CD8 T-cell proliferation was associated with higher TGF-β1 levels and increased percentages of T cells with a gut-homing phenotype at least 15 years after HIV infection during the perinatal period.

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Human immunodeficiency virus type-1 envelope glycoprotein gp120 induces expression of fusion regulatory protein (FRP)-1/CD98 on CD4 + T cells: a possible regulatory mechanism of HIV-induced syncytium formation

Medical Microbiology and Immunology ◽

10.1007/s004300050036 ◽

1997 ◽

Vol 185 (4) ◽

pp. 237-243 ◽

Cited By ~ 4

Author(s):

Shigeru Suga ◽

Masato Tsurudome ◽

Masahiro Ito ◽

Shinji Ohgimoto ◽

Nobutada Tabata ◽

...

Keyword(s):

Human Immunodeficiency Virus ◽

T Cells ◽

Human Immunodeficiency Virus Type ◽

Envelope Glycoprotein ◽

Regulatory Mechanism ◽

Regulatory Protein ◽

Syncytium Formation ◽

Immunodeficiency Virus ◽

Glycoprotein Gp120

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Effects of Lymphocyte Isolation and Timing of Processing on Detection of CD127 Expression on T Cells in Human Immunodeficiency Virus-Infected Patients

Clinical and Diagnostic Laboratory Immunology ◽

10.1128/cdli.12.1.228-230.2005 ◽

2005 ◽

Vol 12 (1) ◽

pp. 228-230 ◽

Cited By ~ 7

Author(s):

Jeanette Higgins ◽

Julia A. Metcalf ◽

Randy A. Stevens ◽

Michael Baseler ◽

Martha C. Nason ◽

...

Keyword(s):

Flow Cytometry ◽

Human Immunodeficiency Virus ◽

Clinical Trials ◽

T Cells ◽

Peripheral Blood Mononuclear Cell ◽

Peripheral Blood Mononuclear ◽

Functional Studies ◽

Immunodeficiency Virus ◽

Multicenter Clinical Trials ◽

Cd127 Expression

ABSTRACT Decreases in the detection of CD127 expression on T cells of human immunodeficiency virus-infected patients by flow cytometry can occur by delayed processing or by peripheral blood mononuclear cell isolation and cryopreservation. These observations should be considered in the interpretation of functional studies and the planning of multicenter clinical trials.

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Autoantibodies against CD4 cells are associated with CD4 helper defects in human immunodeficiency virus-infected patients

Blood ◽

10.1182/blood.v77.1.133.bloodjournal771133 ◽

1991 ◽

Vol 77 (1) ◽

pp. 133-140

Author(s):

R Weimer ◽

V Daniel ◽

R Zimmermann ◽

K Schimpf ◽

G Opelz

Keyword(s):

Human Immunodeficiency Virus ◽

T Cells ◽

B Cell ◽

Hiv Positive ◽

Cd4 Cells ◽

T Subsets ◽

Immunodeficiency Virus ◽

Hiv Negative ◽

Autoantibody Formation

To investigate whether autoantibodies against CD4-positive lymphocytes might induce helper dysfunction, autoantibody formation and T-cell function was examined simultaneously in 61 hemophilia patients. Twenty patients were human immunodeficiency virus (HIV)-negative, 26 HIV- positive stage CDC II or III, and 15 were HIV-positive stage CDC IV. T lymphocytes, CD4-positive, or CD8-positive T subsets were cocultured with B lymphocytes and pokeweed mitogen (PWM) for 6 days and Ig- secreting cells were assessed in a reverse hemolytic plaque assay. The presence of IgM, IgG, C3d, or gp120 on the surface of T cells or T subsets was analyzed by flow cytometry. Autoantibodies against CD4- positive T cells were not detected in controls or HIV-negative patients, but were common in HIV-positive patients (20 of 41 patients). In patients with autoantibodies we found an increased incidence of CD4 helper defects (P less than .0001 in CDC II or III patients; P less than .02 in CDC IV patients). 12 of 13 patients with IgM autoantibodies and 4 of 4 with IgG autoantibodies showed CD4 helper defects. Complement fixation had no relevance. Autoantibody formation against CD4 cells was not due to increased in vivo B-cell stimulation (spontaneous plaque formation: 611 +/- 204 PFC/10(6) B cells in autoantibody-negative patients v 650 +/- 202 PFC/10(6) B cells in autoantibody-positive patients; not significant). Thus, our results suggest that autoantibody formation is not caused by a general state of in vivo B-cell activation. Rather, the production of autoantibodies appears to coincide with defects in B-cell proliferation or differentiation, as shown by reduced mitogen-stimulated B-cell responses in CDC II and III patients (P less than .05). Autoantibodies against CD4 cells appear to be involved in the pathogenesis of CD4 helper defects of HIV-infected patients.

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Autoantibodies against CD4 cells are associated with CD4 helper defects in human immunodeficiency virus-infected patients

Blood ◽

10.1182/blood.v77.1.133.133 ◽

1991 ◽

Vol 77 (1) ◽

pp. 133-140 ◽

Cited By ~ 49

Author(s):

R Weimer ◽

V Daniel ◽

R Zimmermann ◽

K Schimpf ◽

G Opelz

Keyword(s):

Human Immunodeficiency Virus ◽

T Cells ◽

B Cell ◽

Hiv Positive ◽

Cd4 Cells ◽

T Subsets ◽

Immunodeficiency Virus ◽

Hiv Negative ◽

Autoantibody Formation

Abstract To investigate whether autoantibodies against CD4-positive lymphocytes might induce helper dysfunction, autoantibody formation and T-cell function was examined simultaneously in 61 hemophilia patients. Twenty patients were human immunodeficiency virus (HIV)-negative, 26 HIV- positive stage CDC II or III, and 15 were HIV-positive stage CDC IV. T lymphocytes, CD4-positive, or CD8-positive T subsets were cocultured with B lymphocytes and pokeweed mitogen (PWM) for 6 days and Ig- secreting cells were assessed in a reverse hemolytic plaque assay. The presence of IgM, IgG, C3d, or gp120 on the surface of T cells or T subsets was analyzed by flow cytometry. Autoantibodies against CD4- positive T cells were not detected in controls or HIV-negative patients, but were common in HIV-positive patients (20 of 41 patients). In patients with autoantibodies we found an increased incidence of CD4 helper defects (P less than .0001 in CDC II or III patients; P less than .02 in CDC IV patients). 12 of 13 patients with IgM autoantibodies and 4 of 4 with IgG autoantibodies showed CD4 helper defects. Complement fixation had no relevance. Autoantibody formation against CD4 cells was not due to increased in vivo B-cell stimulation (spontaneous plaque formation: 611 +/- 204 PFC/10(6) B cells in autoantibody-negative patients v 650 +/- 202 PFC/10(6) B cells in autoantibody-positive patients; not significant). Thus, our results suggest that autoantibody formation is not caused by a general state of in vivo B-cell activation. Rather, the production of autoantibodies appears to coincide with defects in B-cell proliferation or differentiation, as shown by reduced mitogen-stimulated B-cell responses in CDC II and III patients (P less than .05). Autoantibodies against CD4 cells appear to be involved in the pathogenesis of CD4 helper defects of HIV-infected patients.

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Markedly disturbed glutathione redox status in CD45RA+CD4+ lymphocytes in human immunodeficiency virus type 1 infection is associated with selective depletion of this lymphocyte subset

Blood ◽

10.1182/blood.v88.7.2626.bloodjournal8872626 ◽

1996 ◽

Vol 88 (7) ◽

pp. 2626-2633 ◽

Cited By ~ 17

Author(s):

P Aukrust ◽

AM Svardal ◽

F Muller ◽

B Lunden ◽

I Nordoy ◽

...

Keyword(s):

Human Immunodeficiency Virus ◽

T Cells ◽

Oxidized Glutathione ◽

Cd4 Cells ◽

Total Glutathione ◽

Immunodeficiency Virus ◽

Glutathione Redox ◽

Hiv 1 ◽

Cd4 Lymphocytes

We investigated the percentage of CD45RA+ and CD45RO+ T cells in peripheral blood and the intracellular glutathione redox balance in these lymphocyte subsets in patients with human immunodeficiency virus type 1 (HIV-1) infection and healthy controls. In HIV-1-infected patients there was a preferential depletion of CD45RA+CD4+ cells, which was most pronounced in symptomatic patients. In CD4+ lymphocytes from HIV-1-infected patients the glutathione abnormalities were clearly most pronounced in the CD45RA+ subset with a marked increase in level of oxidized glutathione and decreased ratio of reduced to total glutathione as the major characteristics. These abnormalities were shown in CD45RA+ CD4+ lymphocytes from both symptomatic and asymptomatic patients, whereas similar abnormalities in CD45RO+CD4+ cells were found only in symptomatic patients. The glutathione abnormalities in CD45RA+CD4+ lymphocytes were significantly correlated with low numbers of total CD4+ lymphocytes, decreased proportion of CD45RA+CD4+ lymphocytes, and raised serum levels of tumor necrosis factor-alpha. In the CD8+ lymphocytes a decrease in both proportion and absolute numbers of CD45RA+ cells was found, with markedly increased level of oxidized glutathione and decreased ratio of reduced to total glutathione in this subset. These findings suggest that glutathione redox disturbances in CD45RA+ T cells may be of pathogenic importance for the preferential depletion of this subset considered to represent naive T cells, during HIV-1 infection.

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