IL1RAP Antibodies

Background

The IL1RAP gene encodes the interleukin-1 receptor accessory protein, which is an important transmembrane protein mainly expressed on the surface of immune cells and certain tumor cells. This protein acts as a key co-receptor of the IL-1 receptor family and participates in mediating the signal transduction of cytokines such as IL-1 and IL-33, thereby regulating inflammatory responses, immune responses, and hematopoietic processes. Studies have found that IL1RAP is often overexpressed in hematological tumors such as acute myeloid leukemia. It promotes the proliferation and survival of cancer cells by activating downstream NF-κB and MAPK signaling pathways, making it regarded as a potential immunotherapy target. In recent years, monoclonal antibodies targeting IL1RAP and CAR-T therapies have shown anti-tumor effects in preclinical studies, providing a new direction for targeted intervention in related diseases.

Structure Function Application Advantage Our Products

Structure of IL1RAP

The IL1RAP gene encodes an important transmembrane protein with a molecular weight of approximately 80-85 kDa. This value may vary slightly in different cell types depending on the different splicing variants and glycosylation modification states. The following table lists the key characteristics of IL1RAP proteins from different sources:

Species	Human	Mouse	Rat
Molecular Weight (kDa)	Approximately 85	Approximately 82	Approximately 83
Primary Structural Differences	The common receptor for IL-1/IL-33 signaling, a target for cancer treatment	Involved in inflammation and immune regulation, highly homologous to human functions	Often used in the study of neural inflammation and immune related diseases

The IL1RAP protein contains multiple domains. Its core extracellular region is composed of three immunoglobulin-like domains, which are mainly responsible for binding to IL-1 receptors (such as IL1R1) and cytokines. Its transmembrane region and intracellular tail region do not have kinase activity, but through interaction with adaptor proteins such as MyD88, they are crucial for the activation of downstream NF-κB and MAPK signaling pathways. This structural feature makes it a key molecule in regulating innate immune responses and inflammatory processes.

Fig. 1 IL1RAP Blockade: A Novel Therapeutic Strategy to Reduce Atherosclerotic Plaque Burden and Inflammation.¹

Key structural properties of IL1RAP:

Transmembrane co-receptor structure
Extracellular domain-mediated protein interaction
Intracellular domain lacks kinase activity

Functions of IL1RAP

The core function of the IL1RAP protein is to act as a necessary co-receptor of the interleukin-1 receptor family. It not only regulates inflammatory responses but also participates in a variety of important pathological and physiological processes.

Function	Description
Inflammatory Signal Transduction	It forms functional receptor complexes by binding to IL-1R1 or IL-33R, initiating MyD88-dependent NF-κB and MAPK signaling pathways, which are key nodes in the innate immune response.
Immune Cell Activation	It is expressed on the surface of immune cells such as mast cells and macrophages, mediating the activation, proliferation and cytokine release triggered by IL-1 and IL-33.
Tumor Promotion	It is highly expressed in various leukemia and solid tumors. By continuously activating pro-survival signaling pathways, it supports the proliferation, resistance, and immune evasion of cancer cells.
Hematopoietic Regulation	It functions in hematopoietic stem cells and progenitor cells, influencing their proliferation and differentiation, and is related to the occurrence and development of hematological diseases such as myeloproliferative disorders.
Neuroinflammation involvement	Expressed in central nervous immune cells such as microglia, it participates in the neuroinflammatory responses in neurodegenerative diseases and brain injuries.

The signal transduction of IL1RAP exhibits a "dual-effect switch" characteristic: On one hand, its intracellular domain has no catalytic activity on its own and relies entirely on adaptor proteins to transmit signals; on the other hand, its expression level and subcellular localization strictly regulate the intensity and specificity of IL-1 family signaling, making it an important intervention target in the treatment of inflammation and tumors.

Applications of IL1RAP and IL1RAP Antibody in Literature

1. Mulholland, Megan, et al. "Interleukin-1 receptor accessory protein blockade limits the development of atherosclerosis and reduces plaque inflammation." Cardiovascular Research 120.6 (2024): 581-595. https://doi.org/10.1093/cvr/cvae046

Studies have shown that the use of novel antibodies to block IL1RAP can significantly reduce the burden of atherosclerotic plaques and inflammation in mice, and decrease the expression of factors related to white blood cell recruitment. IL1RAP is a key co-receptor in the IL-1, IL-33, and IL-36 signaling pathways, and its inhibition provides a new target for the treatment of atherosclerosis.

2. Métois, Arnaud, et al. "IL1RAP is an immunotherapeutic target for normal karyotype triple-mutated acute myeloid leukemia." Biomarker Research 13.1 (2025): 61. https://doi.org/10.1186/s40364-025-00769-z

This study found that IL1RAP is highly specifically expressed on the surface of NKt-AML leukemia cells, and is associated with poor prognosis and transplant resistance in patients. The IL1RAP antibody can induce its internalization, suggesting its potential as a target for antibody-drug conjugates in treatment.

3. Badi, Yusef Eamon, et al. "IL1RAP expression and the enrichment of IL‐33 activation signatures in severe neutrophilic asthma." Allergy 78.1 (2023): 156-167. https://doi.org/10.1111/all.15487

The study found that the gene signatures activated by IL-33 were significantly enriched in the sputum of patients with neutrophilic and mixed granulocytic asthma, which was associated with the high expression of the IL1RAP co-receptor, suggesting that anti-IL-33 therapy should be extended to the T2 low-type asthma population.

4. Zhang, Yang, et al. "Innate immune mediator, Interleukin-1 receptor accessory protein (IL1RAP), is expressed and pro-tumorigenic in pancreatic cancer." Journal of Hematology & Oncology 15.1 (2022): 70. https://doi.org/10.1186/s13045-022-01286-4

The study found that IL1RAP is widely expressed in pancreatic cancer and its high expression is associated with poor prognosis. Knockdown of IL1RAP can significantly inhibit the growth and invasion ability of cancer cells, and the downstream IRAK4 inhibitor is effective in slowing tumor progression in preclinical models.

5. Zettergren, Anna, et al. "Association of IL 1 RAP-related genetic variation with cerebrospinal fluid concentration of Alzheimer-associated tau protein." Scientific reports 9.1 (2019): 2460. https://doi.org/10.1038/s41598-018-36650-3

The study found that the IL1RAP gene variation has no direct correlation with the risk of Alzheimer's disease, but specific SNPs (such as rs9877502) are significantly associated with the level of tau protein in the cerebrospinal fluid of patients, suggesting that this gene may affect the intensity of disease progression.

Creative Biolabs: IL1RAP Antibodies for Research

Creative Biolabs specializes in the production of high-quality IL1RAP antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

Custom IL1RAP Antibody Development: Tailor-made solutions to meet specific research requirements.
Bulk Production: Large-scale antibody manufacturing for industry partners.
Technical Support: Expert consultation for protocol optimization and troubleshooting.
Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our IL1RAP antibodies, custom preparations, or technical support, contact us at email.

Reference

Mulholland, Megan, et al. "Interleukin-1 receptor accessory protein blockade limits the development of atherosclerosis and reduces plaque inflammation." Cardiovascular Research 120.6 (2024): 581-595. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.1093/cvr/cvae046