The crucial roles of Th17-related cytokines/signal pathways in M. tuberculosis infection

Interleukin-17 (IL-17), IL-21, IL-22 and IL-23 can be grouped as T helper 17 (Th17)-related cytokines because they are either produced by Th17/Th22 cells or involved in their development. Here, we review Th17-related cytokines/Th17-like cells, networks/signals and their roles in immune responses or...

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Bibliographic Details
Published in:Cellular & molecular immunology 2018-03, Vol.15 (3), p.216-225
Main Authors: Shen, Hongbo, Chen, Zheng W
Format: Article
Language:English
Subjects:
Animals
Antibodies
Antigens
Biomedical and Life Sciences
Biomedicine
Cells
Cytokines
Granulomas
Helper cells
HIV
Human immunodeficiency virus
Humans
Immune response
Immunoglobulins
Immunology
Infections
Interleukin 17
Interleukin 21
Interleukin 22
Interleukin 23
Laboratories
Lungs
Lymphocytes
Lymphocytes T
Medical Microbiology
Microbiology
Microorganisms
Mycobacterium tuberculosis - physiology
Peptides
Review
Roles
Signal Transduction
Stat3 protein
STAT3 Transcription Factor - genetics
STAT3 Transcription Factor - metabolism
Th17 Cells - immunology
Th17 Cells - metabolism
Transcription
Tuberculosis
Tuberculosis - immunology
Tumor necrosis factor-TNF
Vaccine
Virology
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Summary:Interleukin-17 (IL-17), IL-21, IL-22 and IL-23 can be grouped as T helper 17 (Th17)-related cytokines because they are either produced by Th17/Th22 cells or involved in their development. Here, we review Th17-related cytokines/Th17-like cells, networks/signals and their roles in immune responses or immunity against Mycobacterium tuberculosis (Mtb) infection. Published studies suggest that Th17-related cytokine pathways may be manipulated by Mtb microorganisms for their survival benefits in primary tuberculosis (TB). In addition, there is evidence that immune responses of the signal transducer and activator of transcription 3 (STAT3) signal pathway and Th17-like T-cell subsets are dysregulated or destroyed in patients with TB. Furthermore, Mtb infection can impact upstream cytokines in the STAT3 pathway of Th17-like responses. Based on these findings, we discuss the need for future studies and the rationale for targeting Th17-related cytokines/signals as a potential adjunctive treatment.
ISSN:1672-7681
2042-0226
DOI:10.1038/cmi.2017.128