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IL-13

Official Full Name
interleukin 13
Organism
Homo sapiens
GeneID
3596
Background
This gene encodes an immunoregulatory cytokine produced primarily by activated Th2 cells. This cytokine is involved in several stages of B-cell maturation and differentiation. It up-regulates CD23 and MHC class II expression, and promotes IgE isotype switching of B cells. This cytokine down-regulates macrophage activity, thereby inhibits the production of pro-inflammatory cytokines and chemokines. This cytokine is found to be critical to the pathogenesis of allergen-induced asthma but operates through mechanisms independent of IgE and eosinophils. This gene, IL3, IL5, IL4, and CSF2 form a cytokine gene cluster on chromosome 5q, with this gene particularly close to IL4. [provided by RefSeq, Jul 2008]
Synonyms
P600; IL-13;
Bio Chemical Class
Cytokine: interleukin
Protein Sequence
MHPLLNPLLLALGLMALLLTTVIALTCLGGFASPGPVPPSTALRELIEELVNITQNQKAPLCNGSMVWSINLTAGMYCAALESLINVSGCSAIEKTQRMLSGFCPHKVSAGQFSSLHVRDTKIEVAQFVKDLLLHLKKLFREGRFN
Open
Disease
Allergic/hypersensitivity disorder, Asthma, Atopic eczema, Chronic obstructive pulmonary disease, Idiopathic interstitial pneumonitis, Myeloproliferative neoplasm, Oesophagitis, Pulmonary eosinophilia, Systemic sclerosis, Ulcerative colitis, Vasomotor/allergic rhinitis
Approved Drug
1 +
Clinical Trial Drug
13 +
Discontinued Drug
1 +

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Detailed Information

IL-13 is a Th2 cytokine associated with inflammation, first discovered in 1989, with a molecular weight of approximately 10kD. The gene encoding IL-13 consists of 4 exons and 3 introns, located on chromosome 5q31, 12kb upstream of the IL-4 gene. Other cytokine genes in this chromosomal region include those encoding IL-3, IL-5, IL-9, and GM-CSF. This gene encodes an immunoregulatory cytokine primarily produced by activated Th2 cells.

Production and Function of IL-13

IL-13 is mainly secreted by activated TH2 cells, but is also produced by basophils, eosinophils, mast cells, natural killer cells, epithelial cells, smooth muscle cells, fibroblasts, and NK cells. IL-13 can also regulate the functions of IL-13+ ILC2s, mast cells, macrophages, eosinophils, and B cells.

This cytokine participates in several stages of B cell maturation and differentiation. It upregulates CD23 and MHC class II expression, promoting IgE isotype switching in B cells. IL-13 downregulates macrophage activity, thereby inhibiting the production of proinflammatory cytokines and chemokines. IL-13 can directly act on macrophages, driving their differentiation toward the M2 phenotype, thus producing Th2 responses.

Additionally, IL-13 drives beneficial responses such as IgE isotype switching, eosinophil recruitment, mucus production, and muscle contraction. Research has found that this cytokine is crucial for the pathogenesis of allergen-induced asthma, though its mechanism of action is independent of IgE and eosinophils.

Figure 1: A diagram showing IL-13 sources and effects on immune and structural cells in asthma, highlighting cytokine pathways, cell activation, and therapeutic targeting by tralokinumab. Figure 1. Schematic representation of the cellular sources of IL-13 and its effects on immune and structural cells in asthma. (Marone G, et al., 2019)

IL-13 Receptors and Signaling Pathway Regulation

The multiple functions of IL-13 are mediated by a complex receptor system, including IL-4 receptor α (IL-4Rα; CD124) and two additional homologous cell surface proteins: IL-13 receptor α1 (IL-13Rα1; CD213a1) and IL-13 receptor α2 (IL-13Rα2; CD213a2). IL-4 signals through both type I and type II receptors, while IL-13 signals only through type II receptors.

After IL-4 and IL-13 bind to receptors, they can activate tyrosine kinases such as JAK1, JAK2, JAK3, and TYK2, leading to the phosphorylation and activation of STAT6 and STAT3. Activated STAT transcription factor dimers enter the nucleus to regulate the expression of downstream genes. In some cases, IL-13 signaling through IL-13Rα2 results in the phosphorylation of ERK1/2 in a STAT6-independent manner and the formation of the dimeric transcription factor AP-1. Phosphorylated AP-1 translocates to the nucleus and binds to specific DNA elements.

Interestingly, IL-4 also uses IL-4Rα and IL-13Rα1 as receptors, but simultaneously uses IL-4Rα/IL-2γC as a receptor as well. IL-4Rα and IL-13Rα1 exist as homodimers, and after binding with IL-13, can activate three signaling pathways: the Jak/STAT pathway, the PI-3K pathway, and the MAPK pathway. IL-13Rα2 exists in transmembrane, intracellular, and soluble forms. sIL-13Rα2 binds to IL-13 to form a stable complex, blocking the binding of IL-13 to IL-4Rα/IL-13Rα1. Due to its lack of an intracellular domain, it is often considered a decoy receptor.

Relationship Between IL-13 and Diseases

IL-13 and its receptors are involved in regulating allergic inflammation and are associated with the pathogenesis and treatment of cancer, asthma, and allergic diseases. IL-13 plays a key role in skin barrier dysfunction, skin microbiota imbalance, inflammatory cell infiltration, skin fibrosis, and pruritus, making it a critical cytokine in the pathogenesis of atopic dermatitis.

Clinical studies show that IL-13 signaling is associated with the occurrence of inflammatory diseases, including atopic dermatitis, allergic rhinitis, and asthma. Additionally, IL-13 receptors are expressed on various tumor cell lines and are associated with the pathogenesis of malignant tumors. Diseases related to IL-13 include allergic rhinitis and asthma.

IL-13 Targeted Therapeutic Strategies

Currently, four selective IL-13 inhibitors exist at different stages of development or approval:

Dupilumab: A humanized IgG4 monoclonal antibody that can simultaneously block both IL-4 and IL-13 signaling pathways. It has been approved for type 2 asthma and atopic dermatitis patients. Dupilumab targets the IL-4Rα subunit, thereby preventing IL-4 and IL-13-mediated signaling.

Lebrikizumab: A subcutaneous antibody developed by Eli Lilly targeting the IL-13 cytokine. It competes with IL-4Rα for binding to IL-13, thereby preventing the heterodimerization of the IL-4Rα/IL-13Rα1 subunits and blocking the IL-13 pathway. It is a fully human IgG4 that binds to IL-13 and prevents the formation of the IL-13Rα1/IL-4Rα heterodimeric receptor signaling complex, and can be used to treat atopic dermatitis. In November 2023, the EMA approved it for treating moderate to severe AD in adults and adolescents aged 12 and over weighing at least 40 kg who are suitable for systemic therapy. It was approved in the UK in December 2023, in Japan in January 2024, and by the FDA in September.

Tralokinumab: A fully human IgG4 monoclonal antibody developed by Danish LEO Pharma. Although it also targets IL-13, it differs from Lebrikizumab in that Tralokinumab binds to the IL-13 cytokine at an epitope that overlaps with the IL-13Rα receptor binding site, thereby preventing IL-13 from binding to both IL-13Rα1 and IL-13Rα2. It is a fully human IgG4λ that binds to IL-13, preventing it from binding to IL-13 receptors. It has been approved by the EU and the US FDA for treating moderate to severe atopic dermatitis patients. As early as 2021, Tralokinumab was approved by the EMA and FDA for moderate to severe AD.

Eblasakimab: A monoclonal antibody targeting IL13Rα1 to block IL-13 signal transduction, which can be used to treat atopic dermatitis.

In reality, IL-13 was initially a relatively competitive target, with many large pharmaceutical companies working on it. However, as Dupilumab demonstrated such strong advantages, many projects faded away, with only Eli Lilly's Lebrikizumab and LEO's Tralokinumab making it to the end. As a drug target, IL-13 has had to live in the shadow of IL-4R, making it difficult for IL-13-targeted drugs to surpass dupilumab, which targets IL-4R.

References

  1. Marone G, Granata F, Pucino V, et al. The Intriguing Role of Interleukin 13 in the Pathophysiology of Asthma. Front Pharmacol. 2019;10:1387.
  2. Iwaszko M, Biały S, Bogunia-Kubik K. Significance of Interleukin (IL)-4 and IL-13 in Inflammatory Arthritis. Cells. 2021;10(11):3000.
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