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IL1RL1

Official Full Name
interleukin 33
Organism
Homo sapiens
GeneID
90865
Background
The protein encoded by this gene is a cytokine that binds to the IL1RL1/ST2 receptor. The encoded protein is involved in the maturation of Th2 cells and the activation of mast cells, basophils, eosinophils and natural killer cells. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2015]
Synonyms
DVS27; IL1F11; NF-HEV; NFEHEV; C9orf26;
Bio Chemical Class
Cytokine: interleukin
Protein Sequence
MKPKMKYSTNKISTAKWKNTASKALCFKLGKSQQKAKEVCPMYFMKLRSGLMIKKEACYFRRETTKRPSLKTGRKHKRHLVLAACQQQSTVECFAFGISGVQKYTRALHDSSITGISPITEYLASLSTYNDQSITFALEDESYEIYVEDLKKDEKKDKVLLSYYESQHPSNESGDGVDGKMLMVTLSPTKDFWLHANNKEHSVELHKCEKPLPDQAFFVLHNMHSNCVSFECKTDPGVFIGVKDNHLALIKVDSSENLCTENILFKLSET
Open
Disease
Asthma, Atopic eczema, Chronic obstructive pulmonary disease, Respiratory failure
Approved Drug
0
Clinical Trial Drug
6 +
Discontinued Drug
0

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Detailed Information

Interleukin-1 receptor-like 1, or IL1RL1, is a member of the interleukin-1 receptor family, which is crucial for immunological reactions. Part of a cytokine receptor gene cluster including IL1R1, IL1R2, and IL1RL2, this gene is on chromosome 2q12. Pro-inflammatory triggers cause IL1RL1 to be produced, making it especially important for the activation of helper T cells, which are vital to the immunological defense of the body. Research has revealed that several transcript variants produced by alternative splicing of IL1RL1 help to increase its functional variety.

IL1RL1 is a receptor for the cytokine IL-33 in terms of its signaling function. Contributing to tissue homeostasis and reactions to environmental stimuli, this receptor is essential for both innate and adaptive immunity.

The Role of IL1RL1 in Immunity and Signaling Pathways

IL1RL1 mostly acts as a receptor for IL-33, a cytokine that participates in many immunological activities. Activated by IL-33, IL1RL1 creates a receptor complex with the signaling-required IL1RAP. This system activates MAPK3/ERK1, MAPK1/ERK2, MAPK14, and MAPK8 by recruiting MYD88, IRAK1, IRAK4, and TRAF6, hence starting many immunological responses.

A model of IL-33/ST2 signaling is shown in Figure 1.Figure 1. A model for IL-33/ST2 signaling. (Kakkar R, et al., 2008)

Particularly for the development of T-helper cells, especially Th2 cells, which participate in allergic reactions, this signaling cascade is crucial. IL-33 signaling via IL1RL1 has also been demonstrated to influence tissue healing as well as the immunological reaction to environmental stresses. Studies further indicate that IL1RL1 might affect the production of macrophages that resolve inflammation, hence supporting tissue repair after damage.

Interestingly, certain IL1RL1 isoforms have contradictory effects. While one isoform increases IL-33 signaling, another can decrease it. This dual function emphasizes the intricacy of IL1RL1 in immunological activity.

IL1RL1 in Disease Mechanisms

IL1RL1's participation in several illnesses emphasizes its major function in immune control and inflammation. Some of the illnesses linked to IL1RL1 signaling are listed here:

Allergic Diseases: Its role in allergic illnesses, especially asthma, is among the most researched facets of IL1RL1 activity. By encouraging the activation and recruitment of Th2 cells, IL-33 via IL1RL1 plays a key role in the evolution and aggravation of asthma. Key actors in allergic inflammation are cytokines released by these cells: IL-4, IL-5, and IL-13. Asthma sufferers' airways have been found to have higher amounts of IL-33 and its receptor IL1RL1, hence reinforcing their main involvement in the condition.

Genetic research has also connected changes in the IL1RL1 gene to vulnerability to asthma and other allergy diseases. These results imply that altering IL1RL1 signaling can provide treatment options for controlling allergy disorders.

Chronic Inflammatory Diseases: Chronic inflammatory disorders such chronic obstructive pulmonary disease (COPD) have also been connected to IL1RL1. Smoking and infections cause an inflammatory reaction in the lungs in COPD, and IL-33 expression is observed to be raised in the lungs of sufferers. By interacting with IL1RL1, IL-33 helps to aggravate inflammation, hence causing airway remodeling and advancing the condition. Animal model studies have revealed that inhibiting IL-33 signaling lowers COPD severity, hence suggesting its use as a treatment target.

Cancer: Studies now coming to light have also shown IL1RL1's participation in cancer, especially in relation to tumor microenvironments. IL-33 has been demonstrated to encourage cancer cell invasion and tumor angiogenesis—the creation of new blood vessels—by means of IL1RL1. This implies that IL1RL1 might be involved in the development of certain malignancies. Though its function in the immune regulation of the tumor microenvironment is still being studied, it offers hope as a possible target for cancer immunotherapy.

Autoimmune Diseases: In autoimmune illnesses like rheumatoid arthritis, IL1RL1 and IL-33 add to the inflammation and immunological dysregulation found in afflicted tissues. Released in reaction to cellular injury, IL-33 stimulates immune cells via IL1RL1, hence encouraging inflammatory reactions. Autoimmune diseases' IL1RL1 expression points to its possible use as a biomarker for illness progression and maybe a target for treatment as well.

Future Directions and Potential Therapeutic Implications

Given the important part IL1RL1 plays in controlling immune responses and inflammation, targeting this receptor or its signaling pathways seems to be a treatment option. For example, IL-33 and IL1RL1 suppression might provide fresh paths for managing allergy illnesses, chronic inflammatory disorders, autoimmune diseases, and certain malignancies.

Recent developments in immunotherapy have drawn attention to the possibility of altering cytokine receptors such as IL1RL1. Monoclonal antibodies aimed at IL-33 or its receptor, for example, have demonstrated potential in both preclinical and clinical research. These treatments might control improper immune reactions and relieve chronic inflammation linked to diseases including asthma and COPD.

Furthermore, knowing the dual character of IL1RL1's function—some isoforms encouraging and others suppressing signaling—could help one create more exact therapies. More study is required to completely clarify the processes by which IL1RL1 and IL-33 affect illness etiology and how this understanding may be converted into successful treatments.

References:

  1. Shakerian L, Kolahdooz H, Garousi M, et al. IL-33/ST2 axis in autoimmune disease. Cytokine. 2022;158:156015.
  2. Zhou Y, Xu Z, Liu Z. Role of IL-33-ST2 pathway in regulating inflammation: current evidence and future perspectives. J Transl Med. 2023;21(1):902. Published 2023 Dec 11.
  3. Kakkar R, Lee RT. The IL-33/ST2 pathway: therapeutic target and novel biomarker. Nat Rev Drug Discov. 2008;7(10):827-840.
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