Interleukin-3 and interleukin-17 do not play a dynamic role in the immunopathogenesis of osteoarticular tuberculosis.
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Histopathology
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Part of the susceptibility to tuberculosis has a genetic basis, which is clear in primary immunodeficiencies, but is less evident in apparently immunocompetent subjects. Immune responses were analysed in blood samples from tuberculosis patients and their healthy first-degree relatives who were infected in vitro with mycobacteria (either Mycobacterium tuberculosis or M. bovis BCG). The antimicrobial activity against M. tuberculosis in blood from relatives was significantly lower than that observed in healthy controls. Tuberculosis patients exhibited a higher number of neutrophils, and monocyte phagocytosis was inhibited in both relatives and tuberculosis patients. A remarkable finding was that the production of reactive oxygen species by infected neutrophils was higher in relatives than in healthy controls. A higher production of TNFα in infected blood from relatives was also observed. These results may indicate that relatives display a stronger inflammatory response and that their immune response to M. tuberculosis is different from those of unrelated controls. First-degree relatives may represent a highly informative group for the analysis of tuberculosis susceptibility.
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Critical to the complete expression of the virulence of M. tuberculosis and thereby its pathogenesis in human infection, is the ability of this pathogen to interact with the host in a specific manner. To date, cytokine circuits during tuberculosis and M. tuberculosis infection have been studied most intensely. With this regard, both the whole M. tuberculosis and its protein and non-protein moieties appear to be influential on the in situ cytokine profile, and consequently, to the final outcome of infection. The interplay and final balance of macrophage activating and immuno-enhancing cytokines versus macrophage deactivating and immunosuppressive cytokines most likely determines the final expression of M. tuberculosis infection. Further, cytokine circuits also underlie the immunopathology of tuberculosis. Modulation of the in vivo cytokine milieu may allow the development of more effective vaccines to prevent M. tuberculosis infection, and adjunctive immunotherapy to improve treatment of tuberculosis.
Pathogenesis
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Host-pathogen interactions in tuberculosis should be studied at the disease site because Mycobacterium tuberculosis is predominately contained in local tissue lesions. Although M. tuberculosis infection involves different clinical forms of tuberculosis, such as pulmonary tuberculosis, pleural tuberculosis, and lymph node tuberculosis, most studies of human tuberculosis are performed using cells from the peripheral blood, which may not provide a proper reflection of the M. tuberculosis-specific immune responses induced at the local site of infection. A very low proportion of M. tuberculosis-specific effector T cells are found in the blood compared with the infected tissue, and thus there may be considerable differences in the cellular immune response and regulatory mechanisms induced in these diverse compartments. In this review, we discuss differences in the immune response at the local site of infection compared with the peripheral circulation. The cell types and immune reactions involved in granuloma formation and maintenance as well as the in situ technologies used to assess local tuberculosis pathogenesis are also described. We need to strengthen and improve the exploratory strategies used to dissect immunopathogenesis in human tuberculosis with the aim to accelerate the implementation of relevant research findings in clinical practice.
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Summary The adaptive immune response mediated by T cells is critical for control of Mycobacterium tuberculosis ( M. tuberculosis ) infection in humans. However, the M. tuberculosis antigens and host T‐cell responses that are required for an effective adaptive immune response to M. tuberculosis infection are yet to be defined. Here, we review recent findings on CD 4 + and CD 8 + T‐cell responses to M. tuberculosis infection and examine the roles of distinct M. tuberculosis ‐specific T‐cell subsets in control of de novo and latent M. tuberculosis infection, and in the evolution of T‐cell immunity to M. tuberculosis in response to tuberculosis treatment. In addition, we discuss recent studies that elucidate aspects of M. tuberculosis ‐specific adaptive immunity during human immunodeficiency virus co‐infection and summarize recent findings from vaccine trials that provide insight into effective adaptive immune responses to M. tuberculosis infection.
Tuberculosis vaccines
Cellular immunity
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SUMMARY Fifty years after the introduction of the first effective antimicrobial agents against Mycobacterium tuberculosis, this pathogen continues to be a tremendous public health problem. The rise in the number of resistant strains and the difficulties involved in the therapy of tuberculosis in immunocompromised AIDS patients have renewed the interest in the development of effective vaccines. To evaluate whether a potential vaccine against tuberculosis could prevent infection by eliciting a protective antibody response, we reviewed the history of antibody-mediated immunity against tuberculosis. Review of the literature of the past 100 years demonstrates that there is sufficient evidence to conclude that antibody-mediated immunity can modify the course of infection in certain situations. Based on our findings and on what is known in other systems, we propose that the role of antibody-mediated immunity to M. tuberculosis be reexamined, using advanced technology.
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Inflammation plays a crucial role in the control of Mycobacterium tuberculosis infection. In this study, we demonstrate that an inflammatory pulmonary environment at the time of infection mediated by lipopolysaccharide treatment in mice confers enhanced protection against M. tuberculosis for up to 6 months postinfection. This early and transient inflammatory environment was associated with a neutrophil and CD11b
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Interferon-gamma(IFN-γ) is a kind of cytokine with the effects of anti-virus,anti-tumor and immunoregulation,and it has a close relationship with the occ-urrence,development,outcome,diagnosis and treatment of tuberculosis.In recent years,the role of IFN-γ in the immune incidence of tuberculosis gains attention.It is the key Th1-type cytokine which can control the infection of Mycobacterium tuber-culosis.Based on its special role in anti-tuberculosis immunity,IFN-γ has been used for the diagnosis and immunotherapy of tuberculosis.The following overview is focused on the research progress about the role of IFN-γ in the anti-TB immunity,IFN-γ gene and tuberculosis susceptibility,in vitro interferon gamma release assay for diag nosis of tuberculosis,and the adjuvant effect to tuberculosis of IFN-γ,in order to provide a reference for the prevention,diagnosis and treatment of tuberculosis.
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Globally, about 36.7 million people were living with HIV infection at the end of 2015. The most frequent infection co-occurring with HIV-1 is Mycobacterium tuberculosis—374,000 deaths per annum are attributable to HIV-tuberculosis, 75% of those occurring in Africa. HIV-1 infection increases the risk of tuberculosis by a factor of up to 26 and alters its clinical presentation, complicates diagnosis and treatment, and worsens outcome. Although HIV-1-induced depletion of CD4 + T cells underlies all these effects, more widespread immune deficits also contribute to susceptibility and pathogenesis. These defects present a challenge to understand and ameliorate, but also an opportunity to learn and optimize mechanisms that normally protect people against tuberculosis. The most effective means to prevent and ameliorate tuberculosis in HIV-1-infected people is antiretroviral therapy, but this may be complicated by pathological immune deterioration that in turn requires more effective host-directed anti-inflammatory therapies to be derived.
Pathogenesis
AIDS-Related Opportunistic Infections
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ABSTRACT It has not been fully elucidated which of the components of the immune response against Mycobacterium tuberculosis is indicative of resistance or susceptibility. The aim of this study was to identify an immune parameter that could be indicative of either resistance or susceptibility to M. tuberculosis infection. We prospectively studied (three determinations, at months 0, 8, and 12) 15 patients with chronic pulmonary tuberculosis and 42 healthy individuals with a recent and frequent contact with tuberculosis patients. Peripheral blood mononuclear cells were stimulated with a whole-protein extract or the 30-kDa antigen of M. tuberculosis for 6 days, and several immune parameters were determined. No consistent differences between tuberculosis patients and healthy controls were detected in most immune parameters studied, including the expression of different activation antigens, cytokine secretion, lymphocyte proliferation, and nitric oxide production. However, the synthesis of tumor necrosis factor alpha, the intracellular detection of gamma interferon, and the apoptosis of monocytes under certain culture conditions tended to show clear-cut differences in cells from patients and controls ( P < 0.05 in all cases for most determinations). Nevertheless, when results were analyzed on an individual basis, it was evident that a significant degree of overlapping of values from patients and controls occurred for all parameters studied. We conclude that although the immune parameters tested do not allow the identification of individuals susceptible to M. tuberculosis , the specificity and sensitivity of some of them could be improved through future studies.
Tuberculosis diagnosis
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Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis. Protection against and pathogenesis of tuberculosis greatly depend on specific T lymphocytes, and it is generally assumed that CD4+ T cells — through lymphokine-mediated macrophage activation — are the major mediators of the host response to tuberculosis. In the present report, results from experimental tuberculosis studies in mice are summarized which indicate that both CD4+ and CD8+ T lymphocytes are generated during tuberculosis. Furthermore, evidence is presented that both T cell populations are involved in protection against and pathogenesis of tuberculosis and that the final outcome of the host response depends on an intricate balance between these two types of T cells.
Pathogenesis
Cellular immunity
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