Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026918 (Mycobacterium)
 52,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well known that the activation of cell mediated immunity has an important role in the pathogenesis of pulmonary tuberculosis and the production of the protective immunity against Mycobacterium tuberculosis. During the activation of T-cell by Interleukin-1 released from the macrophage, not only Interleukin-2 but also the soluble Interleukin-2 receptor (sIL-2R) molecule is released into the extracellular fluid. In vitro study reveals that the level of this sIL-2R is well correlated with the degree of activation of the T-cell. We therefore carried out this study to evaluate the significance of the serum IL-2R level in determining the disease activity of pulmonary tuberculosis. The level of sIL-2R was measured by sandwich ELISA method. The level of sIL-2R in 42 patients with bacteriologically -proven active pulmonary tuberculosis (29 far and moderately advanced pulmonary tuberculosis, age: 30.3 +/- 10.3 yrs; 13 minimal pulmonary tuberculosis, age: 34.4 +/- 15.3 yrs) was 1111 +/- 424 mu/ml, which was significantly higher than the normal control group (age: 31.0 +/- 9.9 yrs) (365 +/- 143 mu/ml) and inactive pulmonary tuberculosis group (age: 37.3 +/- 16.9 yrs) (465 +/- 131 mu/ml). But there was no significant difference between 29 patients with advanced pulmonary tuberculosis (1138 +/- 405 mu/ml) and 13 patients with minimal pulmonary tuberculosis (1051 +/- 474 mu/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum levels of soluble interleukin-2 receptor in pulmonary tuberculosis. 227 10

Since the precise mechanism of host responses to infection with Mycobacterium-avium complex (MAC) is unclear and since cytotoxic lymphocytes may be involved in the destruction of cells infected with intracellular pathogens, we investigated the ability of normal peripheral blood lymphocytes to kill MAC-infected monocytes in a short-term isotope release assay. Nylon wool-passed lymphocytes lysed MAC-infected but not uninfected monocytes during a 4-hr assay. Infected monocytes were less sensitive to cell-mediated killing than the standard natural killer (NK) cell-sensitive cell line K562, although the kinetics of lysis were similar. The release of lymphocyte-derived mediators such as tumor necrosis factor, interleukin-2 (IL-2), and interferon-alpha and -gamma could not be implicated as a cause of monocyte death. Through the use of cell-specific monoclonal antibodies plus complement, the phenotype of the effector cell was that of an NK cell (CD3 negative, partially CD8 negative, and CD16 positive). The use of highly purified, negatively selected NK cells confirmed these results. NK cell-mediated lysis of infected monocytes decreased MAC viability, indicating that this cytotoxic activity would not favor dissemination of the organism. The killing of MAC-infected monocytes was reduced by K562 cells, suggesting that these targets shared common recognition/binding structures. These results suggest that NK-cell function may be important in the prevention of or response to MAC infection and may help explain the predilection of AIDS patients to develop widespread disease.
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PMID:Natural killer cell-mediated lysis of Mycobacterium-avium complex-infected monocytes. 231 68

Intradermal (i.d.) immunization of Lewis rats with autoclaved Mycobacterium leprae resulted in antigen-specific proliferation responses and interleukin-2 release from spleen and lymph node cells that were detectable as early as 21 days, persisted for at least 9 months, and were dependent on the dose of antigen administered. Immunized animals were also completely resistant to a footpad challenge with viable M. leprae. In contrast, intravenous (i.v.) administration of at least 10(8) irradiated M. leprae isolates induced a state of nonresponsiveness characterized by the absence of proliferation and interleukin-2 release by antigen-stimulated lymphoid cell cultures; however, in vitro responses to mitogenic stimulation and in vivo responses to keyhole limpet hemocyanin and Listeria monocytogenes were normal. Animals that received an i.v. injection of M. leprae remained nonresponsive to M. leprae antigens even after a subsequent i.d. immunization. This state of nonresponsiveness persisted for at least 6 months after induction. Results of footpad challenge experiments showed that the ability of animals rendered nonresponsive by an i.v. injection of M. leprae to control the growth of viable M. leprae in the footpad was not different from that of untreated rats. In addition, animals receiving an initial i.v. injection and a subsequent i.d. immunization with M. leprae were not protected from a viable challenge, as were rats that received only i.d. immunization. These results suggest that i.v. administration of a large dose of M. leprae to rats induces a state of nonresponsiveness to M. leprae antigens that may be similar to that seen in lepromatous leprosy patients.
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PMID:Induction of antigen-specific immunity and tolerance to Mycobacterium leprae in Lewis rats. 240 73

Inguinal lymph node lymphocytes from BALB/c mice immunized intradermally with 10(8) 60Co-irradiated Mycobacterium leprae were cloned by limiting dilution culture. In general, cloned T-cell lines exhibited helper type activity producing interleukin-2, macrophage activation factor and gamma-interferon and lines were further characterized in terms of their cross-reactivities with other species of mycobacteria. M. leprae clones derived after a period of in vitro restimulation were found to cross-react with other species of mycobacteria probably recognizing non-specific or closely related common cell wall associated mycobacterial determinants. On the other hand, lines established by cloning directly from immune mice appeared more M. leprae-specific, exhibiting antigen-dependent lymphokine production and proliferation in vitro.
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PMID:Investigation of antigen cross-reactivity of Mycobacterium leprae-reactive murine T-cell lines and clones. 242 43

We have found that natural killer (NK) cells were very active in pleural effusions containing Mycobacterium tuberculosis. Cytotoxicity against K562 and Raji was augmented when the mononuclear cells were cocultured for 18 hr with purified protein derivative (PPD) derived from M. tuberculosis culture supernatants. In pleural effusions of cancer patients, PPD-activated mononuclear cells were less cytotoxic than their counterparts in peripheral blood. However, in the same patients, interferon and interleukin-2 production was greater in pleural effusions than in peripheral blood. On the other hand, in tuberculosis patients there was no significant difference in cytotoxicity between peripheral blood and pleural effusion mononuclear cells, but the production of interferon and interleukin-2 was higher in pleural effusions than in peripheral blood. Neither group of patients consistently demonstrated a correlation between production of interferon or interleukin-2 in peripheral blood and cytotoxicity. Both PPD-induced cytotoxicity and the production of interferon and interleukin-2 were lower in mononuclear cells of carcinomatous than tuberculous pleural effusion. These results indicate that peripheral blood and pleural effusion mononuclear cells differ in cytotoxicity as well as in interferon and interleukin-2 production. Further, these activities also differ in tuberculous and carcinomatous pleural effusions.
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PMID:Purified protein derivative induced cytotoxicity in carcinomatous and tuberculous pleurisy. 246 59

A high molecular weight protein from Mycobacterium tuberculosis (M. tuberculosis) has been identified, that is recognized by peripheral blood mononuclear cells from several tuberculous patients and by a T cell clone derived from a patient with tuberculous pleurisy. Purification of this fraction demonstrated biological activity to reside in a 180-kDa protein component. This mycobacterial protein appears to exist in some, but not all mycobacteria as the clone reacts to M. tuberculosis, BCG M. kansasii, M. flavescens and M. fortuitum, but not to M. intracellulare, M. scrofulaceum or a variety of gram-positive or gram-negative bacteria, or to PPD. Specific anti-genic challenge of the T cell clone in the presence of irradiated antigen presenting cells results in proliferation and interleukin-2 (IL-2) production. Proliferation is restricted to HLA Class II antigens as antigenic recognition occurs only in the presence of either one of the two parental DR haplotypes. Peripheral blood mononuclear cells from several other patients with pulmonary tuberculosis also proliferate in response to this antigen, emphasizing the relevance of T cell cloning techniques in identifying important mycobacterial antigens.
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PMID:A 180-kilodalton protein from Mycobacterium tuberculosis defined by a human T cell clone. 248 13

Serum from Mycobacterium bovis BCG-infected mice that had been challenged with lipopolysaccharide (LPS) exhibited a marked ability to induce gamma interferon (IFN-gamma) in cultures of spleen cells of normal mice in the presence of interleukin-2 (IL-2). The inducing activity became detectable in the circulatory system about 90 min after LPS challenge, disappeared at around 5 h, and was observable upon 640x dilution of the serum. Addition of monoclonal anti-IL-2 receptor antibody to the culture inhibited the induction by the serum. The activity induced high levels of IFN-gamma even in nylon wool-nonadherent cells, while concanavalin A failed to do so. Serum from uninfected mice challenged with LPS contained no such activity. The molecular weight of the active substance, estimated by gel filtration, was about 70,000. There were pronounced differences among mouse strains in the activities of the sera prepared, which paralleled the amounts of IFN-gamma produced in vivo. However, the levels of IFN-gamma produced in whole spleen cells and in nylon wool-nonadherent cells from mice of various strains were the same when stimulated with competent serum. These results indicate the existence of an unidentified factor that induces IFN-gamma in cooperation with IL-2 in macrophage-depleted splenocytes. They also suggest that IFN-gamma production in vivo is not genetically controlled at the lymphocyte level but, rather, at the level of synthesis of the unknown factor.
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PMID:Endotoxin-induced serum factor that stimulates gamma interferon production. 249 65

Gamma interferon, an immune lymphokine that protects mouse macrophages against infection by several parasites, was ineffective against Mycobacterium lepraemurium. On the contrary, it significantly stimulated multiplication of M. lepraemurium in the macrophages. Simultaneous treatment of macrophages with gamma interferon and interleukin-4 or interleukin-2 or a combination of all three did not enhance the macrophage resistance to infection with M. lepraemurium, but instead stimulated growth of M. lepraemurium.
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PMID:Enhancement of growth of Mycobacterium lepraemurium in macrophages by gamma interferon. 250 Dec 20

We have previously shown that concanavalin A (ConA) induction of suppressor cell activity is impaired in patients with lepromatous leprosy (LL). In this study, we demonstrated that the proportion of cells bearing the Leu8 antigen (associated with suppressor-inducer cells) is low in LL patients and tends to normalize during the erythema nodosum leprosum (ENL) episode. Antigen-induced suppressor cell function was evaluated by a two-stage assay. In the first stage, peripheral blood mononuclear cells (PBMC) were cultured for 5 days either in the presence of gamma-irradiated Mycobacterium leprae or in tissue culture medium as a control. In the second stage, mitomycin C-treated suppressor or control cells were added to phytohemagglutinin (PHA)- or ConA-stimulated autologous PBMC. The results indicate that the ability of M. leprae to induce suppressor activity was lower in LL patients than in patients with tuberculoid (TT) and intermediate clinical (BB, BL, BT) forms and Mycobacterium bovis BCG-immunized normal controls. In ENL patients, the percent suppression was between that of TT and normal individuals. M. leprae-induced suppression was more effective on ConA- than on PHA-triggered T-cell proliferation in all groups. In contrast, normal PBMC cultured for 5 days in RPMI 1640 medium (N-C) and cells from patients with leprosy (TT-C and LL-C) had effects of their own on PHA- or ConA-induced proliferation. LL-C depressed the response to ConA and enhanced PHA-induced proliferation of autologous cells. Conversely, TT-C reduced PHA-induced proliferation and increased the ConA response. Suppression of proliferation could not be overcome with exogenous interleukin-2 and was not related to the induction of the Tac antigen. The abilities of LL, TT, ENL, and normal cells to proliferate upon PHA or ConA stimulus were similar, indicating that the defect in the generation of in vitro suppression by M. leprae in LL patients occurred during the induction period (step 1 of assay).
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PMID:Reduced suppressor cell response to Mycobacterium leprae in lepromatous leprosy. 252 41

Although the immunologic role of T cells bearing the conventional alpha beta T cell receptor (TCR) has been well characterized, little is known about the function of the population of T cells bearing the gamma delta TCR. Therefore, the role of gamma delta T cells in the immune response to Mycobacterium tuberculosis (MT) was investigated. The number of TCR gamma delta cells in the draining lymph nodes of mice immunized with MT was greatly increased in comparison with the number of TCR alpha beta cells. Three biochemically distinct gamma delta TCRs were detected. Analyses of cell cycle, of interleukin-2 receptor expression, and of interleukin-2 responsiveness showed that a large proportion of the gamma delta T cells were activated in vivo. TCR gamma delta cells responded to solubilized MT antigens in vitro but, in contrast to MT-specific alpha beta T cells, the response of gamma delta T cells to MT did not require major histocompatability complex class II recognition. These results provide an example of antigen-specific activation of gamma delta T cells in vivo and indicate that gamma delta T cells may have a distinct role in generating a primary immune response to certain microorganisms.
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PMID:Activation of gamma delta T cells in the primary immune response to Mycobacterium tuberculosis. 252 98


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