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Interactions between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Autoimmune
Bas C Mourik1, Erik Lubberts2, Jurriaan E M de Steenwinkel1
1Department of Medical Microbiology and Infectious Diseases, Erasmus University Medical Center, Rotterdam, Netherlands.
Frontiers in Immunology
|April 21, 2017
Summary
The classical view of tuberculosis (TB) immunity is challenged by new research. Type 1 interferons and Th17 responses, studied in autoimmune diseases, offer new insights into TB pathogenesis.
Area of Science:
- Immunology
- Infectious Diseases
- Autoimmune Diseases
Background:
- The traditional Th1-centric model of tuberculosis (TB) immunity is insufficient, as vaccine strategies targeting Th1 responses have yielded poor results.
- Increased lung interferon-gamma (IFN-γ) levels in preclinical TB models exacerbate host damage rather than control the pathogen.
- Type 1 interferon signaling and altered Th17 responses are linked to active TB, but their precise roles in disease progression require elucidation.
Purpose of the Study:
- To review the roles of type 1 interferons and Th17 immunity in TB pathogenesis.
- To explore interactions between type 1 interferon and Th17 responses observed in systemic autoimmune diseases (AID).
- To evaluate the relevance of these AID-related pathways for a novel perspective on TB research.
Main Methods:
- Literature review focusing on type 1 interferons, Th17 immunity, and their interactions in TB and AID.
- Analysis of functional interactions including effects on monocytes, B-cell activating factor production, and tertiary lymphoid structures.
- Discussion of the roles of GM-CSF-secreting Th17.1 cells, neutrophils, and follicular helper T-cells.
Main Results:
- Type 1 interferons and Th17 immunity have complex roles in TB, potentially contributing to pathogenesis.
- Interactions between type 1 interferon and IL-17 signaling influence monocyte and neutrophil functions.
- Synergistic effects of IL-17 and type 1 interferons are observed in tertiary lymphoid structure formation and follicular helper T-cell responses.
Conclusions:
- Rethinking TB immunity beyond the classical Th1 paradigm is necessary.
- Investigating type 1 interferon and Th17 pathways, informed by autoimmune disease research, offers new avenues for understanding TB.
- These insights may lead to novel therapeutic and vaccine strategies for tuberculosis.
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