Interleukin-22 receptor

From WikiMD's Wellness Encyclopedia

Interleukin-22 receptor (also known as IL-22R) is a type of protein that in humans is encoded by the IL22RA1 gene. It is a part of the cytokine receptor family, specifically the class II cytokine receptor family. The IL-22R is involved in several immune system processes and plays a crucial role in the body's response to inflammation and infection.

Structure[edit | edit source]

The IL-22R is a heterodimeric receptor composed of two subunits: IL-22RA1 and IL-10R2. The IL-22RA1 subunit is unique to the IL-22R, while the IL-10R2 subunit is shared with other members of the class II cytokine receptor family. The IL-22RA1 subunit is responsible for the specific binding of IL-22, while the IL-10R2 subunit is involved in signal transduction.

Function[edit | edit source]

The primary function of the IL-22R is to bind to IL-22, a cytokine produced by T cells and innate lymphoid cells. This binding triggers a cascade of intracellular signaling events that lead to the activation of the JAK-STAT signaling pathway, which in turn regulates the expression of genes involved in inflammation, cell proliferation, and cell survival.

In addition to its role in immune responses, the IL-22R is also involved in tissue repair and regeneration. It is expressed in various tissues, including the skin, liver, and respiratory tract, where it promotes the production of antimicrobial peptides and stimulates the proliferation of epithelial cells.

Clinical significance[edit | edit source]

Abnormalities in the function or expression of the IL-22R have been associated with several diseases, including psoriasis, rheumatoid arthritis, and inflammatory bowel disease. In these conditions, the overproduction of IL-22 leads to excessive activation of the IL-22R, resulting in chronic inflammation and tissue damage. Conversely, deficiencies in IL-22 or the IL-22R can impair the body's ability to fight off infections and heal damaged tissues.

See also[edit | edit source]

References[edit | edit source]

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