Modulatory effect of Tim-3/Galectin-9 axis on T-cell-mediated immunity in pulmonary tuberculosis

Protection againstMycobacterium tuberculosisis based on cell-mediated immunity, most importantly involvingCD4+andCD8+T-cell subsets. The aim of this study was to evaluateCD4+andCD8+T-cell profiles andCD19+andCD3-CD(16+56)+populations in patients with pulmonary tuberculosis.CD4+andCD8+T cells, B-lymphocytes, and natural killer (NK) cells were evaluated in 75 active (APTB) and 25 inactive (IPTB) pulmonary tuberculosis cases and 20 healthy subjects (HCs). The results were compared at different stages of antituberculosis treatment in the APTB patients and also according to X-ray findings in the newly diagnosed APTB patients. The percentages ofCD4+T cells were significantly lower(P<.01)and those ofCD3-CD(16+56)+cells were significantly higher(P<.01)in APTB patients than in HCs.CD8+T cells were significantly decreased(P<.05), andCD3-CD(16+56)+cells were significantly increased(P<.01), in IPTB patients compared to HCs. The percentages ofCD4+,CD8+,CD3-CD19+, andCD3-CD(16+56)+cells showed no differences at different times of the antituberculosis regimen, and different stages of newly diagnosed APTB patients. APTB patients have a reduced percentage of circulatingCD4+T cells and an increased percentage of NK cells compared with healthy individuals. These cells could play important roles in the immune response toM tuberculosisinfection.

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T Lymphocyte Polyclonal Proliferation and Stress Response Style

Psychological Reports ◽

10.1177/0033294187060003-221.1 ◽

1987 ◽

Vol 60 (3_part_2) ◽

pp. 1121-1122

Author(s):

Edward A. Workman ◽

Mariano F. La Via

Keyword(s):

T Cell ◽

T Lymphocyte ◽

Life Stress ◽

Type A Behavior ◽

Response Style ◽

Cell Mediated Immunity ◽

Behavioral Indices ◽

Cell Immunity ◽

Stress Avoidance ◽

Pearson Correlations

18 subjects were measured on cell-mediated immunity (T lymphocyte polyclonal proliferation) and four behavioral indices including over-all life stress, stress-avoidance tendency, stress-intrusion tendency, and tendency toward cardiovascular Type A behavior. Of Pearson correlations computed between T lymphocyte polyclonal proliferation and each of the four behavioral indices, the only significant value was that, .47, between T cell immunity and tendency toward stress avoidance. Of the variables investigated, the best predictor of T cell immunocompetence is the tendency toward avoiding stress. Results are discussed in terms of implications for research.

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Vitamin D Supplementation Modulates T Cell–Mediated Immunity in Humans: Results from a Randomized Control Trial

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2015-3599 ◽

2016 ◽

Vol 101 (2) ◽

pp. 533-538 ◽

Cited By ~ 18

Author(s):

Gauree Gupta Konijeti ◽

Pankaj Arora ◽

Matthew R. Boylan ◽

Yanna Song ◽

Shi Huang ◽

...

Keyword(s):

Vitamin D ◽

T Cell ◽

Vitamin D Deficiency ◽

T Cell Activation ◽

Vitamin D3 ◽

Cell Activation ◽

Atp Release ◽

High Dose ◽

Cell Mediated Immunity ◽

Ancillary Study

Abstract Context: Although studies have linked vitamin D deficiency with immune-mediated diseases, data demonstrating a direct effect on T-cell function are sparse. Objective: Our objective was to determine whether oral vitamin D3 influences T-cell activation in humans with vitamin D deficiency. Design: This was a single-center ancillary study within Vitamin D Therapy in Individuals at High Risk of Hypertension, a double-blind, multicenter, randomized controlled trial. Setting: This study was undertaken in a single academic medical center. Participants: Adults with vitamin D deficiency and untreated pre- or early stage I hypertension were included. Intervention: In Vitamin D Therapy in Individuals at High Risk of Hypertension, participants were randomized to either low- (400 IU daily) or high- (4000 IU daily) dose oral vitamin D3 for 6 months. In this ancillary study of 38 patients, we measured CD4+ T-cell activation estimated by intracellular ATP release after stimulation of whole blood with plant lectin phytohemagglutinin collected at baseline (pretreatment) and 2-month follow-up. Main Outcome Measure: Determining whether ATP level changes were significantly different between treatment groups was the main outcome measure. Results: Treatment with 4000 IU of vitamin D3 decreased intracellular CD4+ ATP release by 95.5 ng/ml (interquartile range, −219.5 to 105.8). In contrast, 400 IU of vitamin D3 decreased intracellular CD4+ ATP release by 0.5 ng/ml (interquartile range, −69.2 to 148.5). In a proportional odds model, high-dose vitamin D3 was more likely than low-dose vitamin D3 to decrease CD4+ ATP release (odds ratio, 3.43; 95% confidence interval, 1.06–1.11). Conclusions: In this ancillary study of a randomized controlled trial, we found that high-dose vitamin D3 significantly reduced CD4+ T-cell activation compared to low-dose vitamin D3, providing human evidence that vitamin D can influence cell-mediated immunity.

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Quantitative analysis of the CD8 + T–cell response to readily eliminated and persistent viruses

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2000.0647 ◽

2000 ◽

Vol 355 (1400) ◽

pp. 1093-1101 ◽

Cited By ~ 29

Author(s):

P. C. Doherty ◽

J. M. Riberdy ◽

G. T. Belz

Keyword(s):

T Cells ◽

T Cell ◽

Influenza A ◽

Flow Cytometric Analysis ◽

T Cell Response ◽

Basic Question ◽

Cell Mediated Immunity ◽

Specific Response ◽

Turnover Rates

The recent development of techniques for the direct staining of peptide–specific CD8 + T cells has revolutionized the analysis of cell–mediated immunity (CMI) in virus infections. This approach has been used to quantify the acute and long–term consequences of infecting laboratory mice with the readily eliminated influenza A viruses (fluA) and a persistent γherpesvirus (γHV). It is now, for the first time, possible to work with real numbers in the analysis of CD8 + T CMI, and to define various characteristics of the responding lymphocytes both by direct flow cytometric analysis and by sorting for further in vitro manipulation. Relatively little has yet been done from the latter aspect, though we are rapidly accumulating a mass of numerical data. The acute, antigen–driven phases of the fluA and γHV–specific response look rather similar, but CD8 + T–cell numbers are maintained in the long term at a higher ‘set point’ in the persistent infection. Similarly, these ‘memory’ T cells continue to divide at a much greater rate in the γHV–infected mice. New insights have also been generated on the nature of the recall response following secondary challenge in both experimental systems, and the extent of protection conferred by large numbers of virus–specific CD8 + T cells has been determined. However, there are still many parameters that have received little attention, partly because they are difficult to measure. These include the rate of antigen–specific CD8 + T–cell loss, the extent of the lymphocyte ‘diaspora’ to other tissues, and the diversity of functional characteristics, turnover rates, clonal life spans and recirculation profiles. The basic question for immunologists remains how we reconcile the extraordinary plasticity of the immune system with the mechanisms that maintain a stable milieu interieur. This new capacity to quantify CD8 + T–cell responses in readily manipulated mouse models has obvious potential for illuminating homeostatic control, particularly if the experimental approaches to the problem are designed in the context of appropriate predictive models.

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DIFFERENTIAL EFFECTS OF MYELOID DENDRITIC CELLS GENETICALLY ENGINEERED TO EXPRESS VIRAL OR MAMMALIAN IL-10 ON T CELL-MEDIATED IMMUNITY.

Transplantation Journal ◽

10.1097/00007890-200004271-00939 ◽

2000 ◽

Vol 69 (Supplement) ◽

pp. S355

Author(s):

Takuya Takayama ◽

Hideaki Tahara ◽

Angus W. Thomson

Keyword(s):

Dendritic Cells ◽

T Cell ◽

Genetically Engineered ◽

Cell Mediated Immunity ◽

Myeloid Dendritic Cells ◽

Differential Effects

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T-cell-mediated concomitant immunity to syngeneic tumors. I. Activated macrophages as the expressors of nonspecific immunity to unrelated tumors and bacterial parasites.

Journal of Experimental Medicine ◽

10.1084/jem.145.2.275 ◽

1977 ◽

Vol 145 (2) ◽

pp. 275-292 ◽

Cited By ~ 54

Author(s):

R J North ◽

D P Kirstein

Keyword(s):

T Cell ◽

Cell Mediated Immunity ◽

Microbial Infection ◽

Nonspecific Resistance ◽

Normal Test ◽

Concomitant Immunity ◽

Progressive Growth ◽

Concomitant Resistance ◽

Growth Of Tumor ◽

Syngeneic Tumors

Progressive growth of the SA1 sarcoma was shown to result in the generation of a state of concomitant resistance to growth of a second implant of the same tumor. The responding lymph nodes of concomitantly immune mice were shown to contain theta-positive T cells that could specifically neutralize the growth of tumor cells in a normal test recipient. Nevertheless, the concomitantly immune host itself was capable to a limited extent of suppressing the growth of unrelated tumors. The generation of immunity, moreover, was associated with the generation of a powerful state of macrophage-mediated, nonspecific resistance to the bacterial parasite, Listeria monocytogenes. It was concluded that systemic macrophage activation was the consequence of the generation of T-cell-mediated immunity to the progressively growing tumor, and that this not only gave the host the capacity to inhibit the growth of unrelated tumors, but also to protect itself against microbial infection. The results gives credence to the view that macrophages play a central role in defense against microbial and neoplastic growth.

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Modulation of T cell cytokine production by miR-144* with elevated expression in patients with pulmonary tuberculosis

Molecular Immunology ◽

10.1016/j.molimm.2011.02.001 ◽

2011 ◽

Vol 48 (9-10) ◽

pp. 1084-1090 ◽

Cited By ~ 88

Author(s):

Yanhua Liu ◽

Xinjing Wang ◽

Jing Jiang ◽

Zhihong Cao ◽

Bingfen Yang ◽

...

Keyword(s):

T Cell ◽

Pulmonary Tuberculosis ◽

Cytokine Production ◽

Elevated Expression ◽

Cell Cytokine Production

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Immunologically mediated regression of a murine lymphoma after treatment with anti-L3T4 antibody. A consequence of removing L3T4+ suppressor T cells from a host generating predominantly Lyt-2+ T cell-mediated immunity.

Journal of Experimental Medicine ◽

10.1084/jem.168.6.2193 ◽

1988 ◽

Vol 168 (6) ◽

pp. 2193-2206 ◽

Cited By ~ 75

Author(s):

M Awwad ◽

R J North

Keyword(s):

T Cells ◽

T Cell ◽

Tumor Regression ◽

Cell Mediated Immunity ◽

Complete Regression ◽

Suppressor T Cells ◽

Antibody Treatment ◽

P815 Mastocytoma ◽

Thymectomized Mice

This study shows that intravenous injection of 1 mg of anti-L3T4 mAb (GK1.5) into thymectomized mice bearing the syngeneic L5178Y lymphoma results, after a delay of 2-3 d, in complete regression of this tumor and in long-term host survival. A flow cytofluorometric examination of the spleen cells of mAb-treated mice revealed that antibody treatment resulted in the elimination of greater than 98% of L3T4+ T cells, but had no effect on the Lyt-2+ T cells subset. Tumor regression was immunologically mediated, because L5178Y lymphoma cells were shown to be L3T4-, and regression of the tumor failed to occur in mice that had been lethally irradiated before anti-L3T4 mAb was given. Tumor regression was mediated by tumor-sensitized Lyt2+ T cells, as evidenced by the finding that treatment of tumor-bearing mice with anti-Lyt-2 mAb alone, or in combination with anti-L3T4 mAb, resulted in enhancement of tumor growth and a significant decrease in host survival time. Moreover, the spleens of mice whose tumors were undergoing regression in response to anti-L3T4 mAb treatment contained Lyt-2+ T cells capable, on passive transfer, of causing regression of a tumor in recipient mice. These results can be interpreted as showing that removal of tumor-induced L3T4+ suppressor T cells results in the release of Lyt-2+ effector T cells from suppression, and consequently in the generation of enough Lyt-2+ T cell-mediated immunity to cause tumor regression. This can only be achieved, however, if immunity to the tumor is mediated exclusively by Lyt-2+ T cells, as is the case for the L5178Y lymphoma. In the case of the P815 mastocytoma, treatment with anti-L3T4 mAb was without a therapeutic effect, and this was in keeping with the finding that immunity to this tumor is mediated by L3T4+, as well by Lyt-2+ T cells.

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