The many faces of host responses to tuberculosis

Collins, Helen; Kaufmann, Stefan H. E.

doi:10.1046/j.1365-2567.2001.01236.x

Cited by 130 publications

(100 citation statements)

References 80 publications

(124 reference statements)

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“…Such downmodulatory factors are actually anti-inflammatory molecules that are produced to protect against the tissue damage induced by excessive inflammation, but at the same time deregulate protective immunity. 18 Our observations are supported by other investigators that relied on murine models, 21 in vitro stimulated peripheral blood cells of patients 22 or lung cells from induced sputum 23 to show a suppressed immune status was associated with tuberculosis patients. In the current study, using pleurisy fluid from tuberculosis patients, we confirmed and further extended the prior research.…”

Section: Pf Inhibits the Functions Of T Cells And Differentiation Of supporting

confidence: 82%

Pleural fluid from tuberculous pleurisy inhibits the functions of T cells and the differentiation of Th1 cells via immunosuppressive factors

Liu

et al. 2011

Cell Mol Immunol

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Immunosuppressive mediators in tuberculosis pleurisy (pleural fluid (PF)) are associated with the course of disease, but they remain poorly defined. To study the local immune status of patients with tuberculosis pleurisy, we examined the effect of PF on the functions of T cells and the differentiation of Th1 cells. PF could inhibit the ability of T cells to produce cytokines. However, tumor-necrosis factor (TNF)-a derived from non-T cells was not impaired. Further analysis indicated that cell activation and cell cycle progression were also suppressed. Moreover, PF could inhibit Th1 cell differentiation. Importantly, we found that inhibitors of indoleamine 2,3-dioxygenase (IDO) and adenosine and neutralizing antibodies against IL-10 and transforming growth factor (TGF)-b could reverse cytokine production, suggesting that IDO, adenosine, IL-10 and Transforming growth factor-b1 in PF might take part in impairing T-cell functions. Taken together, our data demonstrate for the first time that several immunopathological factors participate in the downregulation of T-cell functions in local PF.

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Section: Pf Inhibits the Functions Of T Cells And Differentiation Of supporting

confidence: 82%

Pleural fluid from tuberculous pleurisy inhibits the functions of T cells and the differentiation of Th1 cells via immunosuppressive factors

Liu

et al. 2011

Cell Mol Immunol

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“…Of the three pathogens that we used, ST is the most virulent and consequently resulted in the maximal erosion of preexisting CD8 ϩ T cell memory, whereas BCG is the least virulent pathogen which induced the least erosion of memory. However, BCG is the most chronic pathogen, as detectable burden is noticeable even at 6 mo postinfection, whereas ST burden declines after day 90 (17,18). LM infection lasts for Ͻ7 days (21) and results in erosion that is greater than that induced by BCG.…”

Section: Discussionmentioning

confidence: 99%

IFN-γ Induces the Erosion of Preexisting CD8 T Cell Memory during Infection with a Heterologous Intracellular Bacterium

Dudani

Krishnan

Sad

2008

The Journal of Immunology

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Memory T cells are critical for the control of intracellular pathogens and require few signals for maintenance; however, erosion of established preexisting memory CD8+ T cells has been shown to occur during infection with heterologous viral infections. We evaluated whether this also occurs during infection with various intracellular bacteria and what mechanisms may be involved. We demonstrate that erosion of established memory is also induced during infection of mice with various intracellular bacteria, such as Listeria monocytogenes, Salmonella typhimurium, and Mycobacterium bovis (bacillus Calmette-Guérin). The extent of erosion of established CD8+ T cell memory was dependent on the virulence of the heterologous pathogen, not persistence. Furthermore, when antibiotics were used to comprehensively eliminate the heterologous pathogen, the numbers of memory CD8+ T cells were not restored, indicating that erosion of preexisting memory CD8+ T cells was irreversible. Irrespective of the initial numbers of memory CD8+ T cells, challenge with the heterologous pathogen resulted in a similar extent of erosion of memory CD8+ T cells, suggesting that cellular competition was not responsible for erosion. After challenge with the heterologous pathogen, effector memory CD8+ T cells were rapidly eliminated. More importantly, erosion of preexisting memory CD8+ T cells was abrogated in the absence of IFN-γ. These studies help reveal the paradoxical role of IFN-γ. Although IFN-γ promotes the control of intracellular bacterial replication during primary infection, this comes at the expense of erosion of preexisting memory CD8+ T cells in the wake of infection with heterologous pathogens.

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“…Too much iron downregulates microbicidal effector mechanisms and favours the growth of the pathogen, whereas too little iron is inhibitory to the induction of antimicrobial processes. 37 However, it is undeniable the importance of iron in the regulation of immune responses. 7,8 The role of genetics in determining lifespan is complex.…”

Section: Discussionmentioning

confidence: 99%

Association between the MHC class I gene HFE polymorphisms and longevity: a study in Sicilian population

et al. 2002

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The many faces of host responses to tuberculosis

Cited by 130 publications

References 80 publications

Pleural fluid from tuberculous pleurisy inhibits the functions of T cells and the differentiation of Th1 cells via immunosuppressive factors

Pleural fluid from tuberculous pleurisy inhibits the functions of T cells and the differentiation of Th1 cells via immunosuppressive factors

IFN-γ Induces the Erosion of Preexisting CD8 T Cell Memory during Infection with a Heterologous Intracellular Bacterium

Association between the MHC class I gene HFE polymorphisms and longevity: a study in Sicilian population

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