| Field | Specification |
|---|---|
| Mfr No | |
| Alternative Names | Interleukin-33|IL-33|Interleukin-1 family member 11|IL-1F11|Nuclear factor from high endothelial venules|NF-HEV|IL33|C9orf26|IL1F11|NFHEV |
| Assay Time | |
| Detection Method | |
| Detection Range | |
| Product Type | |
| Reactivity | |
| Sample Type(s) | Serum, Plasma, Cell Culture Supernatant, cell or tissue lysate, Other liquid samples |
| Sensitivity | |
| Species | |
| Storage | |
| Target | |
| UniProt # |
Background
rat IL-33 (Interleukin-33) is a molecular target commonly studied in immunology and cardiovascular research. Cytokines are secreted signaling proteins that coordinate immune responses and inflammation through receptor-mediated pathways.
Biological role and mechanism
The biological role of IL-33 is typically understood in terms of its molecular category and interaction network. Depending on the model system, it may participate in cell–cell communication, intracellular signaling, enzymatic processing, or regulation of gene expression programs. Mechanistic interpretation is often strengthened by considering upstream regulators and downstream readouts rather than relying on a single marker.
Expression and abundance of IL-33 can vary by tissue, cell type, and physiological state. In many systems, levels are influenced by factors such as developmental stage, immune activation, metabolic status, and cellular stress. Because sample matrix and pre-analytical handling can affect measured concentrations, interpretation is typically strongest when experiments keep collection and processing consistent across groups.
Nomenclature and related terms
IL-33 (Interleukin-33) may also be referenced as Interleukin-33, IL-33, and Interleukin-1 family member 11 in the literature or in databases. When comparing results across studies, confirm that the reported analyte refers to the same molecule, species context, and molecular form (e.g., precursor vs mature protein, or soluble vs membrane-associated forms).
Why it matters in research
- Understanding how IL-33 relates to innate and adaptive immune responses, cytokine signaling networks, host–pathogen interactions, and immune cell activation and trafficking in immunology and cardiovascular research.
- Interpreting shifts in IL-33 levels alongside other pathway components or complementary markers.
- Connecting molecular changes to phenotypes such as inflammation, remodeling, metabolism shifts, or cell-state transitions (context-dependent).
Molecular forms and interpretation
For some targets, isoforms, proteolytic processing, or post-translational modifications (such as phosphorylation or glycosylation) can influence function and apparent abundance. If multiple molecular forms are expected in your model, align interpretation with the form most relevant to the biological question.
Disease and translational relevance
IL-33 has been investigated across diverse physiological and disease contexts, and changes in its abundance have been reported in areas aligned with immunology and cardiovascular studies. These associations are interpreted as research findings rather than diagnostic or therapeutic claims, and they should be evaluated alongside model-specific covariates and study design.
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Unveiling IL-33/ST2 Pathway Unbalance in Cardiac Remodeling Due to Obesity in Zucker Fatty Rats
IF: 6.208 Journal: International Journal of Molecular Sciences Cited Date: 2023-01-29
Delivery of neurotrophin-3 by RVG-Lamp2b-modified mesenchymal stem cell-derived exosomes alleviates facial nerve injury
IF: 4.3 Journal: Human Cell Author: Department of Stomatology, Beijing Hospital of Integrated Traditional Chinese and Western Medicine, Beijing, 100000, China. Cited Date: 2024-06-21
Electroacupuncture Protects Against Post-stroke Cognitive Impairment by Promoting an IL-33/ST2 Axis-Mediated Microglia M2 Polarization
IF: 3.8 Journal: Neurochemical Research Author: Rehabilitation Center, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, 450046, China. Cited Date: 2025-11-28
OLR1 Knockdown Mitigates Traumatic-Hemorrhagic Shock-Induced Liver Injury by Inhibiting the TLR4/MYD88 Pathway and NLRP3 Inflammasome Activation
IF: 1.2 Journal: Molecular Biology Author: Department of Emergency and Critical Care Medicine, Wuxi 9th People’s Hospital Affiliated to Soochow University, Wuxi, 214000, Jiangsu, China Cited Date: 2025-08-01
Unveiling cardiac IL-33/ST2L pathway deregulation in animal model of obesity and cardiovascular disease
IF: Journal: Archivio Istituzionale della Ricerca Author: Universit脿 degli Studi di Milano Cited Date: 2023-10-08