ArticleJournal of neuroinflammation2020
IL-22 hinders antiviral T cell responses and exacerbates ZIKV encephalitis in immunocompetent neonatal mice.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- The role of γδ T cells in flavivirus infections: Insights into immune defense and therapeutic opportunities.PLoS neglected tropical diseases · 2025Review
- Enhancing pathogen identification through AI-assisted metagenomic sequencing.Frontiers in microbiology · 2025Article
- I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024Review
- IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024Review
- Interleukin-22 Contributes to Blood-Brain Barrier Disruption via STAT3/VEGFA Activation inACS infectious diseases · 2024Article
- Article
- Interleukin-22 suppresses major histocompatibility complex II in mucosal epithelial cells.The Journal of experimental medicine · 2023Article
- Novel Therapeutic Nutrients Molecules That Protect against Zika Virus Infection with a Special Note on Palmitoleate.Nutrients · 2022Review
- Interleukin-22 Exerts Detrimental Effects on Salivary Gland Integrity and Function.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundThe Zika virus (ZIKV) outbreak that occurred in multiple countries was linked to increased risk of nervous system injuries and congenital defects. However, host immunity- and immune-mediated pathogenesis in ZIKV infection are not well understood. Interleukin-22 (IL-22) is a crucial cytokine for regulating host immunity in infectious diseases. Whether IL-22 plays, a role in ZIKV infection is unknown.
methodsThe cellular source of IL-22 was identified in IFNAR
resultsWe found that γδ T cells were the main source of IL-22 during ZIKV infection in both the spleen and brain. WT mice began to exhibit weight loss, staggered steps, bilateral hind limb paralysis, and weakness at 10 days post-infection (dpi) and ultimately succumbed to infection at 16-19 dpi. IL-22 deficiency lessened weight loss, moderated the systemic inflammatory response, and greatly improved clinical signs of neurological disease and mortality. ZIKV infection also induced the activation of microglia and astrocytes in vitro. Additional analysis demonstrated that the absence of IL-22 resulted in reduced activation of microglia and astrocytes in the cortex. Although IL-22 displayed a negligible effect on glial cells in vitro, IL-22
conclusionsOur data revealed a pathogenic role of IL-22 in ZIKV encephalitis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.