Requirement for CD4+T Cells in the γδ T Cell Proliferative Response to Daudi Burkitt's Lymphoma

1996 ◽  
Vol 174 (1) ◽  
pp. 19-24 ◽  
Author(s):  
James Burns ◽  
Stephen Lobo ◽  
Breck Bartholomew
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Proliferative Response ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Γδ T Cell ◽  
Cell Proliferative Response

scholarly journals CD40 ligation induces Apo-1/Fas expression on human B lymphocytes and facilitates apoptosis through the Apo-1/Fas pathway.

1995 ◽  
Vol 182 (5) ◽  
pp. 1557-1565 ◽  
Author(s):  
E J Schattner ◽  
K B Elkon ◽  
D H Yoo ◽  
J Tumang ◽  
P H Krammer ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
B Cells ◽  
Programmed Cell Death ◽  
B Cell ◽  
B Lymphocytes ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Cd40 Ligation

The Apo-1/Fas antigen (CD95) mediates programmed cell death of lymphocytes when bound by Fas ligand or anti-Apo-1/Fas antibody. In contrast, the CD40 antigen provides a potent activation and survival signal to B lymphocytes when it is engaged by its T cell ligand (CD40L, gp39) or cross-linked by anti-CD40 antibody. In this study, we use human tonsillar B cells and the Ramos Burkitt's lymphoma B cell line, which serves as a model for human germinal center B lymphocytes, to study the effectors of Apo-1/Fas expression and apoptosis of human B cells. We found that Apo-1/Fas expression was upregulated on both malignant and normal human B lymphocytes after CD40 ligation induced by (a) cognate T helper-B cell interaction mediated by microbial superantigen (SAg); (b) contact-dependent interaction with CD40L+, but not CD40L- Jurkat mutant T cell clones; and (c) monoclonal anti-CD40, but not any of a panel of control antibodies. Enhanced B cell Fas/Apo-1 expression is functionally significant. Coculture of Ramos Burkitt's lymphoma line cells with irradiated SAg-reactive CD4+ T cells with SAg or CD40L+ Jurkat T cells results in B cell apoptosis, evidenced by reduced cell viability and DNA laddering. This process is augmented by the addition of anti-Apo-1/Fas monoclonal antibody, consistent with an acquired susceptibility to Apo-1/Fas-mediated apoptosis. These data support an immunoregulatory pathway in which seemingly contradictory signals involving the B cell proliferation/survival antigen CD40, as well as the Apo-1/Fas molecule, which mediates programmed cell death of lymphocytes, are linked in the process of human B cell activation.

HIV protease inhibitors restore impaired T-cell proliferative response in vivo and in vitro: a viral-suppression–independent mechanism

Blood ◽  
2000 ◽  
Vol 96 (1) ◽  
pp. 250-258 ◽  
Author(s):  
Wei Lu ◽  
Jean-Marie Andrieu
Keyword(s):  
T Cells ◽  
T Cell ◽  
Protease Inhibitors ◽  
Peripheral Blood ◽  
Proliferative Response ◽  
Hiv Protease ◽  
Nucleoside Analogues ◽  
Hiv Protease Inhibitors ◽  
Cell Proliferative Response

In 99 adults infected with human immunodeficiency virus type 1 (HIV-1) who received highly active antiretroviral therapy (HAART) (including 2 nucleoside analogues and 1 or 2 protease inhibitors) for 1 year, CD4+ and CD8+ T cells (including memory and naive subsets) increased similarly among patients with sustained plasma viral load decrease, transient decrease, or no decrease. A linear correlation was observed between the decrease in serum β2-microglobulin concentration (an independent surrogate marker of HIV disease) and the increase in peripheral blood T-cells (CD4+ and CD8+) counts. In vitro, HIV protease inhibitors indinavir and saquinavir (but not nucleoside analogues) enhanced the survival of patients' peripheral blood T cells at doses that are at least 30-fold lower than those required for achieving 90% viral inhibition in the same cultures. This enhanced T-cell survival (which is similar for CD4 and CD8 cells) was associated with a restoration of T-cell proliferative response to immune stimuli. However, neither TCR/CD3-ligation– nor Fas-ligation–triggered apoptosis was affected by either of the 2 protease inhibitors. A reduction in apoptosis observed after prolonged culture of patient T cells in the presence of the protease inhibitors could result from restored T-cell proliferation. These findings explain the discrepancies between virologic and immunologic responses that are increasingly reported in patients receiving HAART, and may provide insights into the pathogenesis of HIV infection.

scholarly journals CD4 T cells play important roles in maintaining IL‐17‐producing γδ T‐cell subsets in naive animals

2011 ◽  
Vol 90 (4) ◽  
pp. 396-403 ◽  
Author(s):  
Jeong‐Su Do ◽  
Anabelle Visperas ◽  
Rebecca L O'Brien ◽  
Booki Min
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
T Cell Subsets ◽  
Γδ T Cell

scholarly journals Induction of interleukin 12 responsiveness is impaired in anergic T lymphocytes.

1994 ◽  
Vol 179 (3) ◽  
pp. 1065-1070 ◽  
Author(s):  
H Quill ◽  
A Bhandoola ◽  
G Trinchieri ◽  
J Haluskey ◽  
D Peritt
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Proliferative Response ◽  
Interleukin 12 ◽  
T Helper 1 ◽  
Ifn Gamma ◽  
Enhanced Production

The cytokine, interleukin 12 (IL-12), stimulates both natural killer cells and T cells to proliferate and to secrete interferon gamma (IFN-gamma). The T cell proliferative response to IL-12 must be induced and is evident after T cell receptor-mediated stimulation. As reported here, tolerant CD4+ T cells and clones, that are anergic for IL-2 production, are also anergic for induction of the proliferative response to IL-12. Murine T helper 1 clones tolerized in vitro, as well as anergic CD4+ T cells isolated from mice tolerized to the Mls-1a antigen (Ag) in vivo, demonstrated defective induction of proliferation to IL-12 upon restimulation with Ag. IL-12-enhanced production of IFN-gamma was observed in both control and anergic cells after Ag/antigen-presenting cell (APC) activation, although total IFN-gamma secretion by anergic cells was less than that produced by control cells, even in the presence of IL-12. These data indicate that T cell clonal anergy results in profound inhibition of proliferative responses, since the autocrine growth factor, IL-2, is not produced, and the APC-derived cytokine, IL-12, is not an effective stimulus for anergic T cell proliferation.

scholarly journals T-Cell Hyporesponsiveness Induced by Activated Macrophages through Nitric Oxide Production in Mice Infected withMycobacterium tuberculosis

1999 ◽  
Vol 67 (7) ◽  
pp. 3221-3226 ◽  
Author(s):  
Shigeki Nabeshima ◽  
Mari Nomoto ◽  
Goro Matsuzaki ◽  
Kenji Kishihara ◽  
Hatsumi Taniguchi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Cell Response ◽  
Cd4 T Cells ◽  
Proliferative Response ◽  
Transforming Growth Factor ◽  
T Cell Response ◽  
Activated Macrophages

ABSTRACT In active tuberculosis, T-cell response to Mycobacterium tuberculosis is known to be reduced. In the course ofMycobacterium tuberculosis infection in mice, we observed that T-cell proliferation in response to M. tuberculosispurified protein derivative (PPD) reached the maximum level on day 7, then declined to the minimal level on day 14, and persisted at a low level through day 28 postinfection. The frequency of PPD-specific CD4 T cells in the spleen on day 28 decreased to one-sixth on day 7. To further investigate the mechanism of this T-cell hyporesponsiveness, we next analyzed the suppressive activity of spleen macrophages on T-cell function. The nonspecific proliferative response of naive T cells and the PPD-specific proliferative response of T cells were suppressed by day 28 macrophages, but not by day 7 macrophages or naive macrophages. This reduction of proliferative response was restored by addition of nitric oxide synthesis inhibitor, NG-monoethyl-l-arginine monoacetate, but not by monoclonal antibody against interleukin 10 or transforming growth factor β. These data indicate that the macrophages from mice chronically infected with M. tuberculosis suppress T-cell response through production of nitric oxide, suggesting that nitric oxide-induced elimination mediated by activated macrophages may reduce the T-cell response and the number of mycobacterium-specific CD4 T cells in vivo.

scholarly journals Δ42PD1-TLR4 Augments γδ-T Cell Activation of the Transitional Memory Subset of CD4+ T Cells

iScience ◽  
2020 ◽  
Vol 23 (10) ◽  
pp. 101620
Author(s):  
Yufei Mo ◽  
Allen Ka Loon Cheung ◽  
Yue Liu ◽  
Li Liu ◽  
Zhiwei Chen
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cd4 T Cells ◽  
Cell Activation ◽  
Γδ T Cell ◽  
Memory Subset

HIV protease inhibitors restore impaired T-cell proliferative response in vivo and in vitro: a viral-suppression–independent mechanism

Blood ◽  
2000 ◽  
Vol 96 (1) ◽  
pp. 250-258 ◽  
Author(s):  
Wei Lu ◽  
Jean-Marie Andrieu
Keyword(s):  
T Cells ◽  
T Cell ◽  
Protease Inhibitors ◽  
Peripheral Blood ◽  
Proliferative Response ◽  
Hiv Protease ◽  
Nucleoside Analogues ◽  
Hiv Protease Inhibitors ◽  
Cell Proliferative Response

Abstract In 99 adults infected with human immunodeficiency virus type 1 (HIV-1) who received highly active antiretroviral therapy (HAART) (including 2 nucleoside analogues and 1 or 2 protease inhibitors) for 1 year, CD4+ and CD8+ T cells (including memory and naive subsets) increased similarly among patients with sustained plasma viral load decrease, transient decrease, or no decrease. A linear correlation was observed between the decrease in serum β2-microglobulin concentration (an independent surrogate marker of HIV disease) and the increase in peripheral blood T-cells (CD4+ and CD8+) counts. In vitro, HIV protease inhibitors indinavir and saquinavir (but not nucleoside analogues) enhanced the survival of patients' peripheral blood T cells at doses that are at least 30-fold lower than those required for achieving 90% viral inhibition in the same cultures. This enhanced T-cell survival (which is similar for CD4 and CD8 cells) was associated with a restoration of T-cell proliferative response to immune stimuli. However, neither TCR/CD3-ligation– nor Fas-ligation–triggered apoptosis was affected by either of the 2 protease inhibitors. A reduction in apoptosis observed after prolonged culture of patient T cells in the presence of the protease inhibitors could result from restored T-cell proliferation. These findings explain the discrepancies between virologic and immunologic responses that are increasingly reported in patients receiving HAART, and may provide insights into the pathogenesis of HIV infection.

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