IL17RB

Official Full Name

interleukin 17 receptor B

Organism

Homo sapiens

GeneID

55540

Background

The protein encoded by this gene is a cytokine receptor. This receptor specifically binds to IL17B and IL17E, but does not bind to IL17 and IL17C. This receptor has been shown to mediate the activation of NF-kappaB and the production of IL8 induced by IL17E. The expression of the rat counterpart of this gene was found to be significantly up-regulated during intestinal inflammation, which suggested the immunoregulatory activity of this receptor. [provided by RefSeq, Jul 2008]

Synonyms

CRL4; EVI27; IL17BR; IL17RH1;

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Detailed Information

The IL17RB gene encodes interleukin-17 receptor B (IL-17RB), a key member of the IL-17 receptor family. IL-17RB is a type I transmembrane protein with an extracellular region containing two characteristic fibronectin type III domains, a structural hallmark that distinguishes this receptor family from other cytokine receptors. While IL17RB shares homology with other family members, such as IL17RA, its ligand-binding specificity is distinct. IL-17RB binds with high affinity to two cytokines: IL-17B and IL-17E (also known as IL-25), with IL-25 being more widely studied due to its unique biological functions. Unlike IL-17A, which predominantly drives proinflammatory responses, IL-17RB signaling, especially via IL-25, predominantly initiates type 2 immune responses.

Biological Significance

The primary biological role of IL17RB is as the dominant receptor for IL-25, acting as a central hub in type 2 immune responses. Type 2 immunity is crucial for defense against large extracellular parasites and forms the pathological basis of allergic inflammation. When IL-25 binds IL17RB on type 2 innate lymphoid cells (ILC2s), Th2 cells, basophils, and epithelial cells, it promotes the formation of a heterodimer with IL17RA, triggering a cytoplasmic signaling cascade. This pathway involves the adaptor protein Act1, recruitment of TNF receptor-associated factors (TRAFs), and activation of transcription factors NF-κB and AP-1, ultimately inducing production of type 2 cytokines such as IL-4, IL-5, and IL-13.

Figure 1. IL-17 Cytokine and Receptor Family. (Amatya N, et al., 2017)

IL-4 and IL-13 stimulate B cells to produce IgE and promote goblet cell hyperplasia and mucus overproduction.

IL-5 is essential for eosinophil activation, proliferation, and chemotaxis.

Thus, the IL17RB/IL-25 axis functions as an alert system, particularly in barrier tissues such as the lungs, skin, and gut, coordinating protective immune programs characterized by IgE elevation, eosinophilia, and mucus secretion. Beyond immune cells, IL17RB is also expressed in various non-immune cells, contributing to tissue repair and remodeling.

Clinical Significance

Clinically, IL17RB is primarily relevant in type 2 immune-mediated diseases, anti-parasitic immunity, and cancer:

Allergic diseases: In conditions such as asthma, atopic dermatitis, and chronic rhinosinusitis with nasal polyps, the IL-25/IL17RB axis is a key driver. Elevated IL-25 in patient airways activates ILC2s and Th2 cells, leading to persistent IL-5 and IL-13 production, eosinophilic inflammation, airway hyperreactivity, and remodeling. Therapeutic strategies targeting IL-25 or IL17RB with monoclonal antibodies are being explored for severe eosinophilic asthma and atopic dermatitis, aiming to block the upstream cytokine cascade.

Anti-parasitic immunity: IL17RB signaling is crucial for clearance of intestinal helminths; pathway defects may impair effective protective immunity.

Cancer: IL17RB plays a context-dependent role. In certain solid tumors, such as breast and pancreatic cancers, IL17RB overexpression correlates with tumor invasion, metastasis, and poor prognosis, potentially via epithelial-mesenchymal transition or by stimulating tumor stemness through autocrine/paracrine signaling. Conversely, IL-25/IL17RB-driven type 2 responses in the tumor microenvironment may suppress anti-tumor type 1 immunity, indirectly facilitating immune evasion. Therefore, clinical strategies targeting IL17RB must be disease-context-specific: inhibiting its signaling in allergic diseases or tumors, but potentially enhancing it in parasitic infections.

References

Rickel EA, Siegel LA, Yoon BR, et al. Identification of functional roles for both IL-17RB and IL-17RA in mediating IL-25-induced activities. J Immunol. 2008;181(6):4299–4310.
Fallon PG, Ballantyne SJ, Mangan NE, et al. Identification of an interleukin (IL)-25-dependent cell population that provides IL-4, IL-5, and IL-13 at the onset of helminth expulsion. J Exp Med. 2006;203(4):1105–1116.
Hams E, Armstrong ME, Barlow JL, et al. IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis. Proc Natl Acad Sci U S A. 2014;111(1):367–372.
Amatya N, Garg AV, Gaffen SL. IL-17 Signaling: The Yin and the Yang. Trends Immunol. 2017 May;38(5):310-322.

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