ArticleGenes and immunity2014
The multiple sclerosis risk gene IL22RA2 contributes to a more severe murine autoimmune neuroinflammation.
Article in Genes and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Control of Intestinal Type 3 Immunity by the Unfolded Protein Response Sensor Inositol-Requiring Enzyme 1α in Antigen-Presenting Cells.Cellular and molecular gastroenterology and hepatology · 2026Article
- Medullary stromal cells define small intestinal lymph node identity in humans and mice.Cell reports · 2025Article
- Lycopene Supplemented Mediterranean Diet Ameliorates Experimental Autoimmune Encephalomyelitis (EAE) in Mice and Changes Intestinal Microbiome.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Supplementation with the Probiotic Strains Bifidobacterium longum and Lactiplantibacillus rhamnosus Alleviates Glucose Intolerance by Restoring the IL-22 Response and Pancreatic Beta Cell Dysfunction in Type 2 Diabetic Mice.Probiotics and antimicrobial proteins · 2025Article
- Is DEXI a Multiple Sclerosis Susceptibility Gene?International journal of molecular sciences · 2025Review
- Modulation of αv integrins by lebecetin, a viper venom-derived molecule, in experimental neuroinflammation and demyelination models.Scientific reports · 2024Article
- Advancing understanding of the role of IL-22 in myelination: insights from the Cuprizone mouse model.Frontiers in neurology · 2024Article
- Neuroinflammation: Extinguishing a blaze of T cells.Immunological reviews · 2022Review
- Temporal overexpression of IL-22 and Reg3γ differentially impacts the severity of experimental autoimmune encephalomyelitis.Immunology · 2021Article
- Optic nerve regeneration screen identifies multiple genes restricting adult neural repair.Cell reports · 2021Article
- Interleukin-22 Influences the Th1/Th17 Axis.Frontiers in immunology · 2021Review
- Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2021Review
- Review
- The RareCells · 2020Article
- Environmental and genetic risk factors for MS: an integrated review.Annals of clinical and translational neurology · 2019Review
- IL-22-binding protein exacerbates influenza, bacterial super-infection.Mucosal immunology · 2019Article
- Interleukin 22 ameliorates neuropathology and protects from central nervous system autoimmunity.Journal of autoimmunity · 2019Article
- Pharmacological Targeting of the ER-Resident Chaperones GRP94 or Cyclophilin B Induces Secretion of IL-22 Binding Protein Isoform-1 (IL-22BPi1).International journal of molecular sciences · 2019Article
- The Interleukin-10 Family of Cytokines and Their Role in the CNS.Frontiers in cellular neuroscience · 2018Review
- The multiple sclerosis risk allele within the AHI1 gene is associated with relapses in children and adults.Multiple sclerosis and related disorders · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Single-nucleotide polymorphisms close to IL22RA2, coding for the soluble interleukin (IL)-22-binding protein (IL-22BP), are strongly and reproducibly associated with multiple sclerosis (MS), but there is little data on how this molecule may affect neuroinflammation. Here, we have studied the mouse ortholog in C57BL/6 wild-type and Il22ra2-deficient mice in the context of experimental autoimmune encephalomyelitis (myelin oligodendrocyte glycoprotein-EAE). In wild-type mice, we demonstrated changes in the levels of transcripts for IL-22, the signaling IL-22 receptor and IL-22BP in lymphoid tissues at the time of T-cell priming and in the inflamed central nervous system (CNS). Because IL-22BP is known to antagonize IL-22 signaling, a primarily pro-inflammatory cytokine, we hypothesized that the Il22ra2-deficient mice would have more severe EAE. Paradoxically, the knockout mice displayed a less severe disease course, less demyelination and less infiltration of immune cells in the CNS. The most straightforward interpretation of our findings is that lack of IL-22BP leads to a higher availability of IL-22, which in the case of CNS inflammation, surprisingly acts in a protective fashion. Thus, deletion of the ortholog of the MS risk gene Il22ra2 in mice has beneficial effects on EAE, which may be considered in new therapeutic strategies for treating neuroinflammation.
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