ArticleScientific reports2017
A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- The potential of IFN-λ, IL-32γ, IL-6, and IL-22 as safeguards against human viruses: a systematic review and a meta-analysis.Frontiers in immunology · 2024Pooled it
- Inhibition of Aryl hydrocarbon receptor Interleukin-22 signaling and worsening of intestinal inflammation byGut microbes · 2026Article
- Neuroimmune Crosstalk in Psoriasis: Mechanisms and Therapeutic Implications.Inflammation · 2025Review
- IL-22 Exacerbates Coxsackievirus Type B3-Induced Pancreatitis by Elevating Viral Replication Through STAT3 Activation.Immune network · 2025Article
- Age-Related Impairment of Innate and Adaptive Immune Responses Exacerbates Herpes Simplex Viral Infection.Pathogens (Basel, Switzerland) · 2025Article
- IL-22 in Atopic Dermatitis.Cells · 2024Review
- Article
- A necroptosis-independent function of RIPK3 promotes immune dysfunction and prevents control of chronic LCMV infection.Cell death & disease · 2023Article
- Transcriptional regulation of innate lymphoid cells and T cells by aryl hydrocarbon receptor.Frontiers in immunology · 2023Review
- IL-33 activates mTORC1 and modulates glycolytic metabolism in CD8Immunology · 2022Article
- Metformin Modulates T Cell Function and Alleviates Liver Injury Through Bioenergetic Regulation in Viral Hepatitis.Frontiers in immunology · 2021Article
- Interleukin-22 Influences the Th1/Th17 Axis.Frontiers in immunology · 2021Review
- Review
- IL-22 hinders antiviral T cell responses and exacerbates ZIKV encephalitis in immunocompetent neonatal mice.Journal of neuroinflammation · 2020Article
- A Double Edged Sword Role of Interleukin-22 in Wound Healing and Tissue Regeneration.Frontiers in immunology · 2020Review
- IL-22 produced by type 3 innate lymphoid cells (ILC3s) reduces the mortality of type 2 diabetes mellitus (T2DM) mice infected with Mycobacterium tuberculosis.PLoS pathogens · 2019Article
- The Interleukin-20 Cytokine Family in Liver Disease.Frontiers in immunology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Interleukin-22 (IL-22) plays an important role in host immunity and tissue homeostasis in infectious and inflammatory diseases. However, the function and regulation of IL-22 in viral infection remain largely unknown. Here, we report that viral infection triggered early IL-22 production from the liver and lymphoid organs. γδ T cells are the main immune cells to produce IL-22 in the liver, a process mediated by the IL-23/phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin complex 1 (mTORC1) signaling pathway. In the presence of IL-23, IL-22 production is independent of aryl hydrocarbon receptor (AhR) signaling. In acute and persistent viral infections, IL-22 deficiency resulted in thymic and splenic hypertrophy, while excessive IL-22 induced atrophy in these lymphoid organs. Moreover, IL-22 deficiency enhanced T cell responses to promote viral clearance, but increased IL-22 in vivo decreased T cell numbers and functions in the liver and lymphoid tissues. Together, our findings reveal a significant effect of the IL-23/PI3K/mTORC1 axis on regulating IL-22 production and also identify a novel role of IL-22 in controlling antiviral T cell responses in the non-lymphoid and lymphoid organs during acute and persistent viral infections.
Indexed as
Identifiers
What OpenQuestion holds
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.