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Chapter 1 : Innate Immune Responses to Tuberculosis

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Abstract:

Tuberculosis (TB) remains one of the leading causes of death by an infectious agent, accounting for approximately 1.3 million deaths per year ( ). Despite its clinical significance, there are still significant gaps in our understanding of pathogenesis and the host mechanisms that limit active disease to approximately 10% of those infected. Nevertheless, we continue to gain insight into the dynamic interplay between pathogen and host, with much of the focus centered on the lung microenvironment because this is the initial and primary site of infection. The lung as the initial “battlefield” provides unique challenges to both the host and pathogen because the host must balance the inflammatory response to limit the damage to lung tissue while inducing a sufficient immune response to control the infection. In contrast, the organism must avoid or circumvent the initial defensive barriers present within the respiratory tract to gain access to its host cell, the alveolar macrophage (AM). The AM response to infection as well as the reaction of other lung immune and nonimmune cells and noncellular components is critical to determining whether the host will directly eliminate the pathogen or will in concert with the acquired immune system develop a protective granulomatous response. In addition, since bacteria disseminate during the early events in infection, engagement of innate immune components outside of the lung is also critical in shaping the host response. These early host processes which constitute the innate immune system will be the focus of this article.

Citation: Schorey J, Schlesinger L. 2017. Innate Immune Responses to Tuberculosis, p 3-31. In Jacobs, Jr. W, McShane H, Mizrahi V, Orme I (ed), Tuberculosis and the Tubercle Bacillus, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.TBTB2-0010-2016
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Figure 1

Schematic of the lung and the role of pulmonary innate immune cells during infection. From left to right: branching of the airways, culminating in the alveolar sacs and the alveolus. Also depicted are the cells in the alveolus. Abbreviations: AEC I and II, type I and II alveolar epithelial cell; AM, alveolar macrophage; DC, dendritic cell; IM, interstitial macrophage; IVM, intravascular macrophage.

Citation: Schorey J, Schlesinger L. 2017. Innate Immune Responses to Tuberculosis, p 3-31. In Jacobs, Jr. W, McShane H, Mizrahi V, Orme I (ed), Tuberculosis and the Tubercle Bacillus, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.TBTB2-0010-2016
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Image of Figure 2
Figure 2

Macrophage receptors known to engage () or its components and the downstream effects of receptor engagement on cytokine production, phagosome-lysosome fusion, and inflammation. Engagement of different receptors results in a macrophage response that can either promote or limit host immunity to infection.

Citation: Schorey J, Schlesinger L. 2017. Innate Immune Responses to Tuberculosis, p 3-31. In Jacobs, Jr. W, McShane H, Mizrahi V, Orme I (ed), Tuberculosis and the Tubercle Bacillus, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.TBTB2-0010-2016
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Figure 3

() fate upon macrophage infection. Following phagocytosis, resides within a modified phagosome which may allow mycobacterial components to enter the cytosol in an ESX-1-dependent manner. The phagosome is also connected to the early endosomal network because membrane compartments can both fuse and bud from the phagosome, allowing exposure to important nutrients such as iron as well as removal of mycobacterial components. Endosomes containing mycobacterial components can fuse with multivesicular bodies (MVBs), leading to their incorporation into intraluminal vesicles, and upon MVB fusion with the plasma membrane, they can be released within exosomes (indicated as red circles in the figure). The phagosome has limited fusion with lysosomes, but with activation by IFN-γ or antibiotic treatment the -containing phagosome may undergo autophagosome formation and following lysosome fusion can limit growth, a process known as autophagy. There are also data suggesting that can escape into the cytosol, although this has been observed in only a limited number of studies.

Citation: Schorey J, Schlesinger L. 2017. Innate Immune Responses to Tuberculosis, p 3-31. In Jacobs, Jr. W, McShane H, Mizrahi V, Orme I (ed), Tuberculosis and the Tubercle Bacillus, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.TBTB2-0010-2016
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Figure 4

Responses of innate immune cells to (), BCG, or their products, demonstrating both the beneficial and detrimental roles these cells have on controlling an infection.

Citation: Schorey J, Schlesinger L. 2017. Innate Immune Responses to Tuberculosis, p 3-31. In Jacobs, Jr. W, McShane H, Mizrahi V, Orme I (ed), Tuberculosis and the Tubercle Bacillus, Second Edition. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.TBTB2-0010-2016
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