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Erschienen in: Inflammation Research 12/2017

15.07.2017 | Review

Striking the right immunological balance prevents progression of tuberculosis

verfasst von: Shachi Pranjal Vyas, Ritobrata Goswami

Erschienen in: Inflammation Research | Ausgabe 12/2017

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Abstract

Introduction

Tuberculosis (TB) caused by infection with Mycobacterium tuberculosis (Mtb) is a major burden for human health worldwide. Current standard treatments for TB require prolonged administration of antimycobacterial drugs leading to exaggerated inflammation and tissue damage. This can result in the reactivation of latent TB culminating in TB progression. Thus, there is an unmet need to develop therapies that would shorten the duration of anti-TB treatment and to induce optimal protective immune responses to control the spread of mycobacterial infection with minimal lung pathology.

Findings

Granulomata is the hallmark structure formed by the organized accumulation of immune cells including macrophages, natural killer cells, dendritic cells, neutrophils, T cells, and B cells to the site of Mtb infection. It safeguards the host by containing Mtb in latent form. However, granulomata can undergo caseation and contribute to the reactivation of latent TB, if the immune responses developed to fight mycobacterial infection are not properly controlled. Thus, an optimal balance between innate and adaptive immune cells might play a vital role in containing mycobacteria in latent form for prolonged periods and prevent the spread of Mtb infection from one individual to another.

Conclusion

Optimal and well-regulated immune responses against Mycobacterium tuberculosis may help to prevent the reactivation of latent TB. Moreover, therapies targeting balanced immune responses could help to improve treatment outcomes among latently infected TB patients and thereby limit the dissemination of mycobacterial infection.
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Metadaten
Titel
Striking the right immunological balance prevents progression of tuberculosis
verfasst von
Shachi Pranjal Vyas
Ritobrata Goswami
Publikationsdatum
15.07.2017
Verlag
Springer International Publishing
Erschienen in
Inflammation Research / Ausgabe 12/2017
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-017-1081-z

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