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At least 55 records · Page 3Linked to original sources
PubMed2006

Selectin ligand-independent priming and maintenance of T cell immunity during airborne tuberculosis.

Immunity to Mycobacterium tuberculosis infection is critically dependent on the timely priming of T effector lymphocytes and their efficient recruitment to the site of mycobacterial implantation in the lung. E-, P-, and L-selectin counterreceptors control lymphocyte homing to lymph nodes and leukocyte trafficking to peripheral sites of acute inflammation, their adhesive function depending on fucosylation by fucosyltransferases (FucT) IV and VII. To address the relative importance of differentially glycosylated selectin counterreceptors for priming of T cell effector functions in a model of mycobacteria-induced granulomatous pulmonary inflammation, we used aerosol-borne M. tuberculosis to infect FucT-IV-/-, FucT-VII-/-, FucT-IV-/-/FucT-VII-/-, or wild-type control mice. In lymph nodes, infected FucT-IV-/-/FucT-VII-/- and, to a lesser extent, FucT-VII-/- mice had severely reduced numbers of T cells and reduced Ag-specific effector responses. By contrast, recruitment of activated T cells into the lungs was similar in all four groups of mice during infection and expression of T cell, and macrophage effector functions were only delayed in lungs of FucT-IV-/-/FucT-VII-/- mice. Importantly, lungs from all groups expressed CXCL13, CCL21, and CCL19 and displayed organized follicular neolymphoid structures after infection with M. tuberculosis, which suggests that the lung served as a selectin ligand-independent priming site for immune responses to mycobacterial infection. All FucT-deficient strains were fully capable of restricting M. tuberculosis growth in infected organs until at least 150 days postinfection. Our observations indicate that leukocyte recruitment functions dictated by FucT-IV and FucT-VII-dependent selectin ligand activities are not critical for inducing or maintaining T cell effector responses at levels necessary to control pulmonary tuberculosis.

Animals↗
PubMed1986

Dissociation of protective immunity against tuberculosis and tuberculin hypersensitivity at a level of lymphokines.

On the basis of present knowledge on the purification and the action mechanisms of macrophage regulating lymphokines, as summarized in Table VIII, tuberculosis immunity and tuberculin delayed type hypersensitivity may be dissociated at a level of responsible lymphokines. Table VIII. Dissociation of TB-IMM and DTH at a level of lymphokine 1. Purification of mediators resulted in separation of MIF/MAF and MCF 2. Anti-MIF antibody has no suppression of MCF reaction 3. Lipid metabolisms of macrophages stimulated with MIF/MAF and MCF are different 4. MIF/MAF suppresses MCF-reaction through monokines.

Animals↗
PubMed1986

Antibody-based enzyme-linked immunosorbent assay for determination of immune complexes in clinical tuberculosis.

Immune complexes were isolated from sera of tuberculosis patients by precipitation with 2.5% polyethylene glycol. The precipitates were characterized by quantitative determination of different immunoglobulin classes by single radioimmunodiffusion, sodium dodecyl sulfate polyacrylamide gel electrophoresis for presence of serum components, Ouchterlony's double diffusion method for detection of complement components C3 and C4, and immuno-dot assay for detection of Mycobacterium tuberculosis antigens. The results showed that polyethylene glycol precipitates of patients' sera were indeed immune complexes, as they contained immunoglobulins, albumin, complement components, and mycobacterial antigens, whereas precipitates from control sera contained mainly albumin. The antibodies present in immune complexes were specific to M. tuberculosis antigen and showed no binding to Escherichia coli antigens. Immune complex levels, as determined by the ability to bind M. tuberculosis antigens in an enzyme-linked immunosorbent assay, were significantly higher in tuberculosis patients (n = 22) than in healthy control subjects (n = 18). Thus, immune complex level could be a useful parameter in the diagnosis of active tuberculosis.

Antibodies↗
PubMed1989

Aging and immunity to tuberculosis: prolonged survival of old mice infected with Mycobacterium tuberculosis by adoptive immunization with memory-immune T lymphocytes.

This study shows that memory immune T lymphocytes, harvested from young (3-month-old) mice infected intravenously with Mycobacterium tuberculosis and then exposed to protracted chemotherapy with isoniazid, are capable of adoptively protecting old (24 month) mice from a subsequent fatal challenge infection. Survival of such adoptively protected animals was prolonged, but did not extend beyond the mean survival time of uninfected old control mice. During this time the passively transferred memory T cell population retained their functional capacity to protect against subsequent tuberculosis infection. These data indicate, therefore, that reconstitution of decayed cell-mediated antimicrobial immunity in old mice in vivo with memory T cells is technically feasible, although the life span of the animal is not extended over that of control animals. They indicate, moreover, that the memory T cells remain functional in what some reports have considered a suppressive environment and show further that the macrophages with which the infused T cells interact in the aged host remain functionally able to express acquired resistance.

Aging↗
PubMed2002

Dendritic cells are decreased in blood and accumulated in granuloma in tuberculosis.

Immunity against tuberculosis consists of innate and adaptive immune responses. In this study, we investigated the dynamics of dendritic cells (DC), which are known to elicit a variety of immune responses, in patients with tuberculosis. CD11c(+) peripheral blood DC were decreased in patients with tuberculosis. Immunohistochemical analyses demonstrated that a number of fascin(+), CD11c(+), HLA-DR(+) DC were infiltrating the lymphocyte areas of the tuberculous granulomas (tubercles). Immunohistochemical analyses also demonstrated that interferon-gamma-producing Th1 cells were increased in the tubercles of the patients, indicating the presence of Th1 polarization at least in the context of inflammatory tissues. In vitro coculture of autologous naive T cells with CD11c(+) or CD11c(-) DC pretreated with Bacillus Calmette Guérin augmented the production of Th1 cells. These findings suggested that the trafficking of DC from the peripheral blood into the tubercles causes a dominant Th1 balance and thus plays an essential role in the immunity against tuberculosis.

CD11c Antigen↗
PubMed1995

[Immune system and pathogenesis of tuberculosis].

Immune characteristics available for 225 patients with active pulmonary tuberculosis were considered with reference to the process severity and progression. Some combinations of immunological parameters reflecting T- and B- cell function proved to provide sufficient information on the disease severity and trends in its progress. Immunological criteria of negative or positive course of tuberculosis vary with prevailing inflammation: productive or exudative. An individual approach should be practiced in reading immunograms which require due regard for immunopathological changes in the lungs.

B-Lymphocytes↗
PubMed1997

Interleukin 12 (IL-12) is crucial to the development of protective immunity in mice intravenously infected with mycobacterium tuberculosis.

Immunity to Mycobacterium tuberculosis infection is associated with the emergence of protective CD4 T cells that secrete cytokines, resulting in activation of macrophages and the recruitment of monocytes to initiate granuloma formation. The cytokine-mediating macrophage activation is interferon-gamma (IFN-gamma), which is largely dependent on interleukin-12 (IL-12) for its induction. To address the role of IL-12 in immunity to tuberculosis, IL-12 p40(-/-) mice were infected with M. tuberculosis and their capacity to control bacterial growth and other characteristics of their immune response were determined. The IL-12 p40(-/-) mice were unable to control bacterial growth and this appeared to be linked to the absence of both innate and acquired sources of IFN-gamma. T cell activation as measured by delayed type hypersensitivity and lymphocyte accumulation at the site of infection were both markedly reduced in the IL-12 p40(-/-) mice. Therefore, IL-12 is essential to the generation of a protective immune response to M. tuberculosis, with its main functions being the induction of the expression of IFN-gamma and the activation of antigen-specific lymphocytes capable of creating a protective granuloma.

Animals↗
PubMed1994

[Quantitative characteristics of immunity in patients with reactivated pulmonary tuberculosis].

Immune status was assessed in 44 patients with pulmonary re-infection tuberculosis using monoclonal antibodies. Quantitative indices of the immune status (relative amount of T-cells, T-helpers, T-suppressors, natural killers) correlated with tuberculosis activity. It is important to identify immunity-compromised subjects among tuberculous patients to rule out relapses with the help of early immunocorrection.

Adult↗