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IL-13 is an immunoregulatory cytokine produced mainly by activated Th2 cells. It plays a central role in allergic inflammation and asthma, acting through mechanisms that can be independent of IgE and eosinophils. IL-13 suppresses macrophage activity, reducing production of proinflammatory cytokines and chemokines. It also regulates B cell maturation and differentiation, upregulates CD23 and MHC class II expression, and promotes IgE class switching. Structurally related to IL-4, IL-5, IL-3, and GM-CSF, IL-13 is part of a cytokine gene cluster on chromosome 5q, located near the IL4 gene.
IL-22 is an alpha-helical cytokine of the IL-10/IFN family, produced primarily by activated T cells (including Th17 cells) and NK cells. The IL22 gene is located on chromosome 12q. IL-22 signals through a heterodimeric receptor composed of IL-22R1 and IL-10R2, activating pathways such as JAK-STAT, particularly STAT3. A soluble receptor, IL-22 binding protein (IL-22BP), can inhibit IL-22 signaling. Unlike many cytokines, IL-22 primarily targets nonimmune cells, including epithelial cells of the skin, gut, and respiratory tract, as well as hepatocytes and keratinocytes. It induces antimicrobial peptides, acute-phase proteins, and promotes tissue repair and wound healing. IL-22 is important for host defense against extracellular pathogens and is highly expressed in chronic inflammatory conditions, where it contributes to tissue inflammation and remodeling.
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