scholarly journals ATP and Control of Intracellular Growth of Mycobacteria by T Cells

2002 ◽  
Vol 70 (11) ◽  
pp. 6456-6459 ◽  
Author(s):  
David H. Canaday ◽  
Reza Beigi ◽  
Richard F. Silver ◽  
Clifford V. Harding ◽  
W. Henry Boom ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Bovis ◽  
Extracellular Atp ◽  
Intracellular Growth ◽  
Human Macrophages ◽  
Bystander Cells ◽  
And Control

ABSTRACT Extracellular ATP at millimolar concentrations inhibits growth of mycobacteria in human macrophages. Whether T cells can produce sufficient ATP is unknown. CD4+ and CD8+ T cells did not release sufficient ATP through either degranulation or lysis of bystander cells to restrict growth of Mycobacterium bovis BCG in monocytes.

scholarly journals β-Glucans inhibit intracellular growth of Mycobacterium bovis BCG but not virulent Mycobacterium tuberculosis in human macrophages

2011 ◽  
Vol 51 (4) ◽  
pp. 233-242 ◽  
Author(s):  
Bret E. Betz ◽  
Abul K. Azad ◽  
Jessica D. Morris ◽  
Murugesan V.S. Rajaram ◽  
Larry S. Schlesinger
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Mycobacterium Bovis ◽  
Intracellular Growth ◽  
Human Macrophages ◽  
Mycobacterium Bovis Bcg

Increased Extracellular ATP in Plasma of Rheumatoid Arthritis Patients Activates CD8+T Cells

2021 ◽  
Author(s):  
Archana Tripathy ◽  
Prasanta Padhan ◽  
Nitish Swain ◽  
Sunil K. Raghav ◽  
Bhawna Gupta
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cells ◽  
Cd8 T Cells ◽  
Extracellular Atp

scholarly journals Early Use of Corticosteroid May Prolong SARS-CoV-2 Shedding in Non-Intensive Care Unit Patients with COVID-19 Pneumonia: A Multicenter, Single-Blind, Randomized Control Trial

Respiration ◽  
2021 ◽  
pp. 1-11
Author(s):  
Xiao Tang ◽  
Ying-Mei Feng ◽  
Ji-Xiang Ni ◽  
Jia-Ying Zhang ◽  
Li-Min Liu ◽  
...  
Keyword(s):  
T Cells ◽  
Randomized Control Trial ◽  
Corticosteroid Treatment ◽  
Clinical Deterioration ◽  
Control Group ◽  
Number Of Patients ◽  
Early Use ◽  
Randomized Control ◽  
And Control ◽  
Single Blind

<b><i>Background:</i></b> There is still no clinical evidence available to support or to oppose corticosteroid treatment for coronavirus disease 2019 (COVID-19) pneumonia. <b><i>Objective:</i></b> To investigate the efficacy and safety of corticosteroid given to the hospitalized patients with COVID-19 pneumonia. <b><i>Methods:</i></b> This was a prospective, multicenter, single-blind, randomized control trial. Adult patients with COVID-19 pneumonia who were admitted to the general ward were randomly assigned to either receive methylprednisolone or not for 7 days. The primary end point was the incidence of clinical deterioration 14 days after randomization. <b><i>Results:</i></b> We terminated this trial early because the number of patients with COVID-19 pneumonia in all the centers decreased in late March. Finally, a total of 86 COVID-19 patients underwent randomization. There was no difference of the incidence of clinical deterioration between the methylprednisolone group and control group (4.8 vs. 4.8%, <i>p</i> = 1.000). The duration of throat viral RNA detectability in the methylprednisolone group was 11 days (interquartile range, 6–16 days), which was significantly longer than that in the control group (8 days [2–12 days], <i>p</i> = 0.030). There were no significant differences between the 2 groups in other secondary outcomes. Mass cytometry discovered CD3<sup>+</sup> T cells, CD8<sup>+</sup> T cells, and NK cells in the methylprednisolone group which were significantly lower than those in the control group after randomization (<i>p</i> &#x3c; 0.05). <b><i>Conclusions:</i></b> From this prematurely closed trial, we found that the short-term early use of corticosteroid could suppress the immune cells, which may prolong severe acute respiratory syndrome coronavirus 2 shedding in patients with COVID-19 pneumonia. <b><i>Trial Registration:</i></b> ClinicalTrials.gov, NCT04273321.

scholarly journals Early Antibody Responses to Experimental Mycobacterium bovis Infection of Cattle

2006 ◽  
Vol 13 (6) ◽  
pp. 648-654 ◽  
Author(s):  
W. R. Waters ◽  
M. V. Palmer ◽  
T. C. Thacker ◽  
J. P. Bannantine ◽  
H. M. Vordermeier ◽  
...  
Keyword(s):  
Mycobacterium Bovis ◽  
Skin Testing ◽  
Rapid Test ◽  
Kinetic Studies ◽  
Immunoblot Analysis ◽  
Immunoglobulin M ◽  
Serum Samples ◽  
Mycobacterial Antigens ◽  
New Generation ◽  
And Control

ABSTRACT Bovine tuberculosis persists as a costly zoonotic disease in numerous countries despite extensive eradication and control efforts. Sequential serum samples obtained from Mycobacterium bovis-infected cattle were evaluated for seroreactivity to mycobacterial antigens. Animals received M. bovis by aerosol, intratonsil, intranasal, or intratracheal inoculation. Assays included the multiantigen print immunoassay for determination of antigen recognition patterns, immunoblot analysis for sensitive kinetic studies, and the VetTB STAT-PAK test, a novel, rapid test based on lateral-flow technology. Responses to MPB83 were detected for all M. bovis-infected animals regardless of the route or strain of M. bovis used for inoculation. Other less commonly recognized antigens included ESAT-6, CFP-10, and MPB70. Responses to MPB83 were detectable as early as 4 weeks after inoculation, were boosted upon injection of purified protein derivatives for skin testing, and persisted throughout the course of each of the four challenge studies. MPB83-specific immunoglobulin M (IgM) was detected prior to MPB83-specific IgG detection; however, early IgM responses rapidly waned, suggesting a benefit of tests that detect both IgM- and IgG-specific antibodies. The VetTB STAT-PAK test detected responses in sera from 60% (15/25) of the animals by 7 weeks after challenge and detected responses in 96% (24/25) of the animals by 18 weeks. These findings demonstrate the potential for new-generation antibody-based tests for the early detection of M. bovis infection in cattle.

scholarly journals CD4+ CD25+ Regulatory T Cells Modulate the T-Cell and Antibody Responses in Helicobacter-Infected BALB/c Mice

2006 ◽  
Vol 74 (6) ◽  
pp. 3519-3529 ◽  
Author(s):  
Maria Kaparakis ◽  
Karen L. Laurie ◽  
Odilia Wijburg ◽  
John Pedersen ◽  
Martin Pearse ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Bacterial Colonization ◽  
Antibody Responses ◽  
T Helper 1 ◽  
Time Of Infection ◽  
Lymph Node Cells ◽  
Antibody Levels ◽  
And Control

ABSTRACT Gastric Helicobacter spp. induce chronic gastritis that may lead to ulceration and dysplasia. The host elicits a T helper 1 (Th1) response that is fundamental to the pathogenesis of these bacteria. We analyzed immune responses in Helicobacter-infected, normal mice depleted of CD4+ CD25+ T cells to investigate the in vivo role of regulatory T cells (Tregs) in the modulation of Helicobacter immunopathology. BALB/c and transgenic mice were depleted of CD4+ CD25+ T cells by administration of an anti-CD25 antibody either at the time of infection with Helicobacter or during chronic infection and gastritis. Depletion of CD25+ Tregs prior to and during infection of mice with Helicobacter spp. did not affect either bacterial colonization or severity of gastritis. Depletion of CD25+ Tregs was associated with increased Helicobacter-specific antibody levels and an altered isotype distribution. Paragastric lymph node cells from CD25+ Treg-depleted and control infected mice showed similar proliferation to Helicobacter antigens, but only cells from anti-CD25-treated animals secreted Th2 cytokines. CD25+ Tregs do not control the level of gastritis induced by gastric Helicobacter spp. in normal, thymus-intact BALB/c mice. However, CD25+ Tregs influence the cytokine and antibody responses induced by infection. Autoimmune gastritis is not induced in Helicobacter-infected mice depleted of CD25+ Tregs but is induced in CD25+ Treg-depleted mice, which have a higher frequency of autoreactive T cells.

scholarly journals Macrophage-dependent Apoptosis of CD4+ T Lymphocytes from HIV-infected Individuals Is Mediated by FasL and Tumor Necrosis Factor

1997 ◽  
Vol 185 (1) ◽  
pp. 55-64 ◽  
Author(s):  
Andrew D. Badley ◽  
David Dockrell ◽  
Margaret Simpson ◽  
Ron Schut ◽  
David H. Lynch ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
T Lymphocytes ◽  
Cd4 T Cells ◽  
Tumor Necrosis ◽  
Human Macrophages ◽  
Infected Cells ◽  
Induced Apoptosis ◽  
Antigen Presenting ◽  
Necrosis Factor

Apoptosis of bystander uninfected CD4+ T lymphocytes by neighboring HIV-infected cells is observed in cell culture and in lymphoid tissue of HIV-infected individuals. This study addresses whether antigen-presenting cells such as human macrophages mediate apoptosis of CD4+ T cells from HIV-infected individuals. Uninfected human macrophages, and to a larger degree, HIV-infected macrophages mediate apoptosis of T cells from HIV-infected, but not from uninfected control individuals. This macrophage-dependent killing targets CD4+, but not CD8+ T lymphocytes from HIV-infected individuals, and direct contact between macrophages and lymphocytes is required. Additional analyses indicated that the apoptosis-inducing ligands, FasL and tumor necrosis factor (TNF), mediate this macrophage-induced apoptosis of CD4+ T cells. These results support a role for macrophage-associated FasL and TNF in the selective depletion of CD4+ T cells in HIV-infected individuals.

scholarly journals Virally Activated CD8 T Cells Home to Mycobacterium bovis BCG-Induced Granulomas but Enhance Antimycobacterial Protection Only in Immunodeficient Mice

2006 ◽  
Vol 75 (3) ◽  
pp. 1154-1166 ◽  
Author(s):  
Laura H. Hogan ◽  
Dominic O. Co ◽  
Jozsef Karman ◽  
Erika Heninger ◽  
M. Suresh ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Mycobacterium Bovis ◽  
Cd8 T Cells ◽  
Bacterial Load ◽  
Granulomatous Inflammation ◽  
Cd8 T Cell ◽  
Activated T Cells ◽  
Immunodeficient Mice ◽  
Ifn Γ

ABSTRACT The effect of secondary infections on CD4 T-cell-regulated chronic granulomatous inflammation is not well understood. Here, we have investigated the effect of an acute viral infection on the cellular composition and bacterial protection in Mycobacterium bovis strain bacille Calmette-Guérin (BCG)-induced granulomas using an immunocompetent and a partially immunodeficient murine model. Acute lymphocytic choriomeningitis virus (LCMV) coinfection of C57BL/6 mice led to substantial accumulation of gamma interferon (IFN-γ)-producing LCMV-specific T cells in liver granulomas and increased local IFN-γ. Despite traffic of activated T cells that resulted in a CD8 T-cell-dominated granuloma, the BCG liver organ load was unaltered from control levels. In OT-1 T-cell-receptor (TCR) transgenic mice, ovalbumin (OVA) immunization or LCMV coinfection of BCG-infected mice induced CD8 T-cell-dominated granulomas containing large numbers of non-BCG-specific activated T cells. The higher baseline BCG organ load in this CD8 TCR transgenic animal allowed us to demonstrate that OVA immunization and LCMV coinfection increased anti-BCG protection. The bacterial load remained substantially higher than in mice with a more complete TCR repertoire. Overall, the present study suggests that peripherally activated CD8 T cells can be recruited to chronic inflammatory sites, but their contribution to protective immunity is limited to conditions of underlying immunodeficiency.

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