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Updated: Jan 18, 2026
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Evaluation of Zika Virus-specific T-cell Responses in Immunoprivileged Organs of Infected Ifnar1-/- Mice
Published on: October 17, 2018
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The IRE1/XBP1s Axis Regulates Innate Immune Responses in Conventional Dendritic Cells During ZIKV Infection
Mónica Guzmán-Rodríguez1, Tomás Hernández-Díaz2,3, Paula Lisboa1
1Immunology Program, Laboratory of Immunology and Cellular Stress, Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile, Santiago, Chile.
Summary
Zika virus (ZIKV) activates conventional dendritic cells (cDCs) via infection, triggering type I interferons and inflammatory cytokines. The IRE1/XBP1s pathway is crucial for this cDC response to ZIKV.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Dendritic cells (DCs) are crucial for antiviral immunity, but their specific role in Zika virus (ZIKV) infection is not fully understood.
- Conventional dendritic cells (cDCs) orchestrate adaptive immunity, yet their response mechanisms to ZIKV require further investigation.
- Previous research primarily focused on monocyte-derived DCs, leaving a knowledge gap regarding cDC activation by ZIKV.
Purpose of the Study:
- To investigate how conventional dendritic cells (cDCs) respond to Zika virus (ZIKV) infection.
- To elucidate the mechanisms of ZIKV-induced activation in cDCs, focusing on cytokine production.
- To identify the specific cDC subset responsible for ZIKV recognition and the signaling pathways involved.
Main Methods:
- Murine cDC cultures were used to study ZIKV infection and activation.
- Flow cytometry was employed to analyze cDC subsets and molecule expression (e.g., CD86).
- Genetic manipulation (loss of XBP1s) was used to assess the role of the IRE1/XBP1s pathway in cDC function.
Main Results:
- ZIKV infection, not just viral detection, activates cDCs, inducing type I interferons (IFN-I) and proinflammatory cytokines.
- ZIKV-infected cDCs strongly activate the IRE1/XBP1s axis of the unfolded protein response (UPR).
- Type 1 cDCs (cDC1s) are identified as the primary ZIKV-sensing subset within cDCs.
- Loss of XBP1s impairs CD86 expression and cytokine production in cDCs without increasing ZIKV susceptibility.
- Tissue-resident cDCs are susceptible to ZIKV infection in vivo.
Conclusions:
- The IRE1/XBP1s pathway is critical for modulating cDC activation in response to ZIKV.
- Viral recognition by cDCs is linked to functional maturation through the IRE1/XBP1s pathway.
- This study highlights the unfolded protein response (UPR) in cDC antiviral defense, suggesting potential therapeutic targets for flavivirus infections.
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