Interleukin 20receptors (IL20R) belong to theIL-10 family. IL20R are involved in bothpro-inflammatory and anti-inflammatory immune response.^[1][2] There are two types of IL20R: Type I and Type II.

IL20R is found in many organ residenteffector cells such askeratinocytes at theskin epidermis,osteoclasts, found in bones, andepithelial cells of theintestine andtrachea. IL20R alpha and beta subunits have also been found in some immune cells.^[2] IL20R is implicated in diseases such aspsoriasis,rheumatoid arthritis, andglaucoma.  

There are two types of IL20R: Type I, made up of theIL-20 receptor alpha subunit andbeta subunit, and Type II, made up of theIL-22 receptor and IL-20 receptor beta subunit.^[3] Both types of receptor bind thecytokinesIL-20,IL-24. Type 1 also binds cytokineIL-19.^[4][5]

IL20R signalling happens through theJAK-STAT pathway.^[4] When an IL-20 subfamily cytokine binds IL20R, JAK's linked to intracellular domains of IL20R activate andphosphorylatetyrosine residues found in the longeralpha chains in the intracellular portion of the receptor.STAT then binds to docking sites created by JAK phosphorylation, and become phosphorylated by JAK's themselves. STATs thendimerize and move to thenucleus to act astranscription factors. The specificgenes expressed are dependent on the specific JAK, STAT, as well as bySOCS proteins, which inhibit the JAK-STAT signal to regulate it.^[3]

STAT3 is the main transcription factor activated with IL20R signaling.^[6]

IL20R subunit genemutations and differences in gene expression are associated with an increased risk ofinflammatory diseases.^[2]

IL20R has is involved in skinhomeostasis. Research shows that IL-20R may play a role in the immune diseasepsoriasis, where rapid growth of skin cells leads to dryness and irritation.^[3] Mutations in IL20R are associated with an increased risk of psoriasis, and psoriatic skin lesions show elevated levels of IL20R.

Under the current understanding of psoriasis, the over-activation ofdendritic cells andmacrophages leads to pro-inflammatory cytokine release, includingTNFα andIL-23. This cytokine release activatesT-helper cells, which produce cytokinesIL-17 andIL-22, and subsequently leads to the release of IL-19 IL-20, and IL-24. The binding of IL-20, IL-24, and IL-19 to IL20R, along with other cytokines binding to their respective receptors, leads to high amounts of keratinocytes. The keratinocytes then lead to psoriatic plaque formation.^[3]

IL20R is linked with rheumatoid arthritis, an autoimmune condition where the immune system attacks joints and other body areas and leads to pain. Elevated levels of IL20R mRNA and proteins are found in people with rheumatoid arthritis. It is thought that production of IL20 which binds to IL20Rs increases the production of chemoattractants, which are immune signaling molecules that can recruit immune cells. The chemoattractants then attract neutrophils and T-cells, which drive inflammation in the joints and cause pain.^[3]

Research also shows that certain gene mutations in IL20R are associated with an increased risk of juvenile idiopathic arthritis.^[2]

Research indicates that IL20Rs, specifically the IL20R beta subunit (IL20RB), may be linked withglaucoma, a disease that can lead toblindness. It's not believed that IL20RB has a causative effect on the disease, but it may contribute to an increased risk of the disease, along with other factors, such asintraocular pressure.^[7]

• Receptors,+Interleukin-20 at the U.S. National Library of MedicineMedical Subject Headings (MeSH)

• Genes on human chromosome 6
• Genes on human chromosome 3
• Type II cytokine receptors

• Protein pages needing a picture