Bioactivation of Latent Transforming Growth Factor β1 by <i>Mycobacterium tuberculosis</i> in Human Mononuclear Phagocytes

Aung, Htin; Wu, Mianda; Johnson, John L.; Hirsch, Christina S.; Toossi, Zahra

doi:10.1111/j.1365-3083.2005.01623.x

Cited by 24 publications

(16 citation statements)

References 29 publications

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“…The effect of CFA is likely due to the presence of Mycobacterium tuberculosis, which strongly activates monocytes to produce TGF-β1 in cell culture (50) and can also convert latent TGF-β1 to its bioactive form (51). Accordingly, these bacteria may be responsible for the observed increase in TGF-β1 production in microglia and astrocytes in our model (Figure 2).…”

Section: Discussionmentioning

confidence: 81%

Glia-dependent TGF-β signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis

Luo¹,

Ho²,

Buckwalter³

et al. 2007

J. Clin. Invest.

109

111

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Autoimmune encephalomyelitis, a mouse model for multiple sclerosis, is characterized by the activation of immune cells, demyelination of axons in the CNS, and paralysis. We found that TGF-β1 synthesis in glial cells and TGF-β-induced signaling in the CNS were activated several days before the onset of paralysis in mice with autoimmune encephalomyelitis. While early production of TGF-β1 was observed in glial cells TGF-β signaling was activated in neurons and later in infiltrating T cells in inflammatory lesions. Systemic treatment with a pharmacological inhibitor of TGF-β signaling ameliorated the paralytic disease and reduced the accumulation of pathogenic T cells and expression of IL-6 in the CNS. Priming of peripheral T cells was not altered, nor was the generation of TH17 cells, indicating that this effect was directed within the brain, yet affected the immune system. These results suggest that early production of TGF-β1 in the CNS creates a permissive and dangerous environment for the initiation of autoimmune inflammation, providing a rare example of the brain modulating the immune system. Importantly, inhibition of TGF-β signaling may have benefits in the treatment of the acute phase of autoimmune CNS inflammation.

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Section: Discussionmentioning

confidence: 81%

Glia-dependent TGF-β signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis

Luo¹,

Ho²,

Buckwalter³

et al. 2007

J. Clin. Invest.

109

111

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“…Most of our knowledge on the role of TGFβ in microbial pathogenesis concerns non-viral pathogens 35, 36 . However, some viruses do cause an increase in TGFβ levels and other viruses express proteins that can cleave and activate TGFβ.…”

Section: Host Factors That Limit Tissue Damagementioning

confidence: 99%

Immunity and immunopathology to viruses: what decides the outcome?

2010

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PREFACE Many viruses infect humans and most are controlled satisfactorily by the immune system with limited damage to host tissues. Some viruses, however, do cause overt damage to the host, either in isolated cases or as a reaction that commonly occurs after infection. The outcome is influenced by properties of the infecting virus, the circumstances of infection and multiple factors controlled by the host. In this Review, we focus on host factors that influence the outcome of viral infection, including genetic susceptibility, the age of the host when infected, the dose and route of infection, the induction of anti-inflammatory cells and proteins as well as the presence of concurrent infections and past exposure to cross-reactive agents.

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“…TGF-β is secreted by a large number of cell types including monocytes, macrophages, DCs, and CD4+ regulatory T cells (Aung et al, 2005; Latchumanan et al, 2005). TGF-β is shown to synergize with IL-10 to promote immune tolerance and limit pathological inflammation (Oswald et al, 1992; Zeller et al, 1999; Clegg and Hughes, 2002; Chen et al, 2003).…”

Section: Immunomodulatory Cytokinesmentioning

confidence: 99%

Mycobacterium Tuberculosis Infection and Inflammation: what is Beneficial for the Host and for the Bacterium?

Sasindran¹,

Torrelles²

2011

Front. Microbio.

216

186

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Tuberculosis is still a major health problem in the world. Initial interactions between Mycobacterium tuberculosis and the host mark the pathway of infection and the subsequent host inflammatory response. This inflammatory response is tightly regulated by both the host and the bacterium during different stages of infection. As infection progresses, the initial intense pro-inflammatory response observed is regulated by suppressive mediators balancing inflammation. In this environment, M. tuberculosis battles to survive interfering with the host inflammatory response. In this review we discuss the major effector molecules involved in inflammation in relation to the different stages of M. tuberculosis infection.

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Bioactivation of Latent Transforming Growth Factor β1 by Mycobacterium tuberculosis in Human Mononuclear Phagocytes

Cited by 24 publications

References 29 publications

Glia-dependent TGF-β signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis

Glia-dependent TGF-β signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis

Immunity and immunopathology to viruses: what decides the outcome?

Mycobacterium Tuberculosis Infection and Inflammation: what is Beneficial for the Host and for the Bacterium?

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