IL1RL1 Specific Neutra™ Antibody Products

Are you struggling with prolonged drug development timelines or challenges in targeting IL1RL1 with high specificity? Creative Biolabs' IL1RL1-specific neutra™ antibody products overcome these hurdles through advanced protein engineering and high-throughput antibody validation, empowering rapid therapeutic candidate discovery and functional characterization of IL1RL1-mediated pathways.

Introduction to IL1RL1

Interleukin 1 receptor-like 1 (IL1RL1), also known as ST2, is a transmembrane receptor belonging to the IL-1 receptor family. It is encoded by the IL1RL1 gene and exists in two primary isoforms: a membrane-bound form (ST2L) and a soluble decoy receptor (sST2). IL1RL1 is primarily expressed on immune cells, including mast cells, Th2 lymphocytes, and macrophages, where it regulates inflammatory and immune responses. Its ligand, interleukin-33 (IL-33), drives IL1RL1 activation, initiating downstream signaling cascades critical in both innate and adaptive immunity.

• Structural Insights

IL1RL1 comprises an extracellular immunoglobulin-like domain, a transmembrane domain, and an intracellular Toll/IL-1 receptor (TIR) domain. The ST2L binds IL-33 with high affinity, triggering dimerization with IL-1 receptor accessory protein (IL-1RAcP) to activate signaling. The soluble isoform (sST2) lacks the transmembrane and TIR domains, serving as a competitive inhibitor by sequestering IL-33. Structural studies reveal that IL1RL1's immunoglobulin domain adopts a β-sheet sandwich fold, enabling precise ligand recognition—a feature exploited in designing neutralizing antibodies.

• Related Signaling Pathways

IL1RL1 activation by IL-33 stimulates the MyD88/NF-κB pathway, promoting pro-inflammatory cytokine production (e.g., IL-6, TNF-α) and Th2-polarized immune responses. Additionally, IL1RL1 signaling modulates MAPK and PI3K-AKT pathways, affecting cell survival, proliferation, and fibrosis. Dysregulation of IL1RL1/IL-33 signaling is implicated in pathologies ranging from asthma to cardiac fibrosis.

Fig. 1 ST2/IL-33 signaling pathway. ¹

• Disease Associations

IL1RL1 is a biomarker and therapeutic target in multiple inflammatory and fibrotic diseases. Elevated sST2 levels correlate with poor prognosis in heart failure, while ST2L overexpression drives asthma, atopic dermatitis, and chronic obstructive pulmonary disease (COPD). In autoimmune disorders like rheumatoid arthritis, IL1RL1 signaling exacerbates tissue damage by amplifying inflammatory cascades.

Applications of Anti-IL1RL1 Neutralizing Antibodies in Clinical Research

• Therapeutic Development for Th2-Driven Diseases

IL1RL1-neutralizing antibodies are pivotal in developing biologics for asthma, COPD, and atopic dermatitis. By blocking IL-33 signaling, these antibodies reduce eosinophil infiltration, mucus hypersecretion, and airway remodeling. Phase II trials targeting severe asthma have shown reduced exacerbation rates and improved lung function.

• Biomarker-guided Treatment in Cardiovascular Diseases

sST2 is a prognostic marker in heart failure, while ST2L inhibition mitigates myocardial fibrosis. Anti-IL1RL1 antibodies are being explored to decelerate disease progression in patients with elevated sST2, offering a dual diagnostic and therapeutic strategy.

• Antifibrotic Therapy for Organ Fibrosis

In idiopathic pulmonary fibrosis (IPF) and hepatic fibrosis, IL1RL1 antibodies inhibit fibroblast-to-myofibroblast transition, reducing collagen deposition. Preclinical data supports their potential to improve tissue architecture and function in progressive fibrotic disorders.

• Immunomodulation in Autoimmune Conditions

Early-stage trials in rheumatoid arthritis and systemic sclerosis demonstrate that IL1RL1 blockade suppresses IL-33-mediated Th2 activation, attenuating synovitis and skin thickening. Combination therapies with existing DMARDs are under investigation to enhance efficacy.

Our Neutralizing Antibodies Targeting IL1RL1

Creative Biolabs' IL1RL1-specific antibodies are developed to disrupt IL-33/IL1RL1 binding with exceptional affinity (K_D < 1 nM) and isoform selectivity. These antibodies recognize epitopes within the IL1RL1 extracellular domain, blocking ligand-induced receptor activation without cross-reactivity to other IL-1 receptor family members. Validated in preclinical models, our antibodies exhibit substantial neutralization in:

-Inflammatory disease models: Suppression of IL-33-driven airway hyperresponsiveness in asthma.

-Fibrosis models: Attenuation of cardiac and pulmonary fibrosis via inhibition of fibroblast activation.

-Autoimmunity: Reduction of joint inflammation in rheumatoid arthritis by modulating Th2 responses.

Our anti-IL1RL1-specific neutra™ antibody products combine unmatched specificity, rigorous validation, and scalable manufacturing to speed your research and therapeutic programs. Contact our scientific team today to explore customized solutions for your IL1RL1-focused projects.

REFERENCE

1. Griesenauer, Brad, and Sophie Paczesny. "The ST2/IL-33 axis in immune cells during inflammatory diseases." Frontiers in immunology 8 (2017): 475. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.3389/fimmu.2017.00475