Expression System: Produced in E. coli with high purity (>95% by SDS-PAGE) and endotoxin levels <1.0 EU/μg .
Amino Acid Sequence: Typically spans residues 31–183 (mature form), excluding the propeptide region. Full-length variants (Met1–Lys183) are also available .
Molecular Weight:
Discrepancies arise from post-translational modifications or buffer components.
ED₅₀: Induces IL-6 secretion in murine NIH/3T3 fibroblasts at 1–10 ng/mL .
Signaling Pathways: Activates NF-κB and MAPK via IL-36R/IL-1Rrp2 and IL-1RAcP coreceptor .
Key Functions:
Skin Inflammation:
Lung Pathology:
COPD/Emphysema: IL-36R knockout mice show reduced neutrophil influx and cytokine production during viral exacerbations .
Arthritis: Synovial fibroblasts and chondrocytes produce IL-6/IL-8 in response to IL-36β stimulation .
Bioassays: Quantifying IL-36β activity via IL-6 induction in NIH/3T3 cells .
ELISA Standards: Carrier-containing formulations ensure stability for quantitative assays .
In Vivo Models: Used to study psoriasis, COPD, and arthritis pathogenesis .
Towne et al. (2004): Demonstrated IL-36β’s role in IL-6/IL-8 induction and NF-κB activation .
Tortola et al. (2012): Linked IL-36β to psoriasiform dermatitis via DC-keratinocyte interactions .
Johnston et al. (2011): Identified IL-36β as a driver of neutrophilic inflammation in lung injury .
Current research explores IL-36β as a therapeutic target in psoriasis and COPD. Neutralizing antibodies and receptor antagonists are under development to mitigate its pro-inflammatory effects while preserving IL-1-mediated host defense .