ArticlePloS one2012
Deletion of IL-33R (ST2) abrogates resistance to EAE in BALB/C mice by enhancing polarization of APC to inflammatory phenotype.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 69 citations in OpenAlex.
- The Role of the IL-33/ST2 Axis in Nervous System Development and Diseases.Immunology and cell biology · 2026Review
- Decreased IL-33 in the brain following repetitive mild traumatic brain injury contributes to cognitive impairment by inhibiting microglial phagocytosis.Military Medical Research · 2025Article
- Targeted proteomics of cerebrospinal fluid in treatment naïve multiple sclerosis patients identifies immune biomarkers of clinical phenotypes.Scientific reports · 2024Article
- Dual roles of interleukin-33 in cognitive function by regulating central nervous system inflammation.Journal of translational medicine · 2022Review
- Targeting the Epithelium-Derived Innate Cytokines: From Bench to Bedside.Immune network · 2022Review
- Functional immune cell-astrocyte interactions.The Journal of experimental medicine · 2021Review
- IL-33 promotes innate lymphoid cell-dependent IFN-γ production required for innate immunity toeLife · 2021Article
- T reg cell-intrinsic requirements for ST2 signaling in health and neuroinflammation.The Journal of experimental medicine · 2021Article
- The NF-κB Transcription Factor c-Rel Modulates Group 2 Innate Lymphoid Cell Effector Functions and Drives Allergic Airway Inflammation.Frontiers in immunology · 2021Article
- Therapeutic Opportunities of Interleukin-33 in the Central Nervous System.Frontiers in immunology · 2021Review
- Type 17 Immune Response Facilitates Progression of Inflammation and Correlates with Cognition in Stable Schizophrenia.Diagnostics (Basel, Switzerland) · 2020Article
- IL-33 and its decoy sST2 in patients with Alzheimer's disease and mild cognitive impairment.Journal of neuroinflammation · 2020Article
- Dual immune functions of IL-33 in inflammatory bowel disease.Histology and histopathology · 2020Review
- The Helminth ParasiteFrontiers in immunology · 2020Article
- Interleukin-17 in Chronic Inflammatory Neurological Diseases.Frontiers in immunology · 2020Review
- Long-term interleukin-33 treatment delays disease onset and alleviates astrocytic activation in a transgenic mouse model of amyotrophic lateral sclerosis.IBRO reports · 2019Article
- Galectin-3 Deficiency Facilitates TNF-α-Dependent Hepatocyte Death and Liver Inflammation in MCMV Infection.Frontiers in microbiology · 2019Article
- Pleiotropic Effects of IL-33 on CD4Frontiers in immunology · 2019Review
- IL-33 receptor (ST2) deficiency downregulates myeloid precursors, inflammatory NK and dendritic cells in early phase of sepsis.Journal of biomedical science · 2018Article
- Innate lymphoid cells in autoimmunity and chronic inflammatory diseases.Seminars in immunopathology · 2018Review
Corrections and comments
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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
The administration of interleukin 33 and deletion of IL-33 receptor, ST2 molecule, affects the induction of autoimmunity in different experimental models of human autoimmune diseases. The aim of this study was to analyze the effect of ST2 deletion on the induction of experimental autoimmune encephalomyelitis (EAE) in resistant BALB/c mice. Mice were immunized with MOG(35-55) peptide or disease was induced by passive transfer of encephalitogenic singenic cells and EAE was clinically and histologically evaluated. Expression of intracellular inflammatory cytokines, markers of activation and chemokine receptors on lymphoid tissue and CNS infiltrating mononuclear cells was analyzed by flow cytometry. We report here that deletion of ST2(-/-) molecule abrogates resistance of BALB/c mice to EAE induction based on clinical and histopathological findings. Brain and spinal cord infiltrates of ST2(-/-) mice had significantly higher number of CD4(+) T lymphocytes containing inflammatory cytokines compared to BALB/c WT mice. Adoptive transfer of ST2(-/-) primed lymphocytes induced clinical signs of the disease in ST2(-/-) as well as in WT mice. MOG(35-55) restimulated ST2(-/-) CD4(+) cells as well as ex vivo analyzed lymph node cells had higher expression of T-bet and IL-17, IFN-γ, TNF-α and GM-CSF in comparison with WT CD4(+) cells. ST2(-/-) mice had higher percentages of CD4(+) cells expressing chemokine receptors important for migration to CNS in comparison with WT CD4(+) cells. Draining lymph nodes of ST2(-/-) mice contained higher percentage of CD11c(+)CD11b(+)CD8(-) cells containing inflammatory cytokines IL-6 and IL-12 with higher expression of activation markers. Transfer of ST2(-/-) but not WT dendritic cells induced EAE in MOG(35-55) immunized WT mice. Our results indicate that ST2 deficiency attenuates inherent resistance of BALB/c mice to EAE induction by enhancing differentiation of proinflammatory antigen presenting cells and consecutive differentiation of encephalitogenic T cells in the draining lymph node rather than affecting their action in the target tissue.
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