IL-25 (IL-17E) in epithelial immunology and pathophysiology
IL-25, also known as IL-17E, is a unique cytokine of the IL-17 family. Indeed, IL-25 exclusively was shown to strongly induce expression of the cytokines associated with type 2 immunity. Although produced by several types of immune cells, such as T cells, dendritic cells, or group 2 innate lymphoid...
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| Veröffentlicht in: | Journal of allergy and clinical immunology 2021-07, Vol.148 (1), p.40-52 |
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| creator | Borowczyk, Julia Shutova, Maria Brembilla, Nicolo Costantino Boehncke, Wolf-Henning |
| description | IL-25, also known as IL-17E, is a unique cytokine of the IL-17 family. Indeed, IL-25 exclusively was shown to strongly induce expression of the cytokines associated with type 2 immunity. Although produced by several types of immune cells, such as T cells, dendritic cells, or group 2 innate lymphoid cells, a vast amount of IL-25 derives from epithelial cells. The functions of IL-25 have been actively studied in the context of physiology and pathology of various organs including skin, airways and lungs, gastrointestinal tract, and thymus. Accumulating evidence suggests that IL-25 is a “barrier surface” cytokine whose expression depends on extrinsic environmental factors and when upregulated may lead to inflammatory disorders such as atopic dermatitis, psoriasis, or asthma. This review summarizes the progress of the recent years regarding the effects of IL-25 on the regulation of immune response and the balance between its homeostatic and pathogenic role in various epithelia. We revisit IL-25’s general and tissue-specific mechanisms of action, mediated signaling pathways, and transcription factors activated in immune and resident cells. Finally, we discuss perspectives of the IL-25–based therapies for inflammatory disorders and compare them with the mainstream ones that target IL-17A. |
| doi_str_mv | 10.1016/j.jaci.2020.12.628 |
| format | Article |
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Indeed, IL-25 exclusively was shown to strongly induce expression of the cytokines associated with type 2 immunity. Although produced by several types of immune cells, such as T cells, dendritic cells, or group 2 innate lymphoid cells, a vast amount of IL-25 derives from epithelial cells. The functions of IL-25 have been actively studied in the context of physiology and pathology of various organs including skin, airways and lungs, gastrointestinal tract, and thymus. Accumulating evidence suggests that IL-25 is a “barrier surface” cytokine whose expression depends on extrinsic environmental factors and when upregulated may lead to inflammatory disorders such as atopic dermatitis, psoriasis, or asthma. This review summarizes the progress of the recent years regarding the effects of IL-25 on the regulation of immune response and the balance between its homeostatic and pathogenic role in various epithelia. We revisit IL-25’s general and tissue-specific mechanisms of action, mediated signaling pathways, and transcription factors activated in immune and resident cells. Finally, we discuss perspectives of the IL-25–based therapies for inflammatory disorders and compare them with the mainstream ones that target IL-17A.</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/j.jaci.2020.12.628</identifier><identifier>PMID: 33485651</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Asthma ; Atopic dermatitis ; Cell cycle ; Chemokines ; chronic rhinosinusitis ; contact dermatitis ; Crohn disease ; Cytokines ; Dendritic cells ; Eczema ; Environmental factors ; Epithelial cells ; Gastrointestinal tract ; Gene expression ; Homeostasis ; idiopathic pulmonary fibrosis ; IL-17E ; IL-25 ; Immunology ; inflammatory bowel disease ; Inflammatory diseases ; Interleukin 17 ; keratinocytes ; Kinases ; Lymphocytes ; Lymphocytes T ; Lymphoid cells ; Phosphorylation ; Proteins ; Psoriasis ; Pulmonary fibrosis ; Recruitment ; Rhinitis ; Signal transduction ; Sinusitis ; Transcription factors ; tuft cells ; ulcerative colitis</subject><ispartof>Journal of allergy and clinical immunology, 2021-07, Vol.148 (1), p.40-52</ispartof><rights>2021</rights><rights>Copyright © 2021. 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Indeed, IL-25 exclusively was shown to strongly induce expression of the cytokines associated with type 2 immunity. Although produced by several types of immune cells, such as T cells, dendritic cells, or group 2 innate lymphoid cells, a vast amount of IL-25 derives from epithelial cells. The functions of IL-25 have been actively studied in the context of physiology and pathology of various organs including skin, airways and lungs, gastrointestinal tract, and thymus. Accumulating evidence suggests that IL-25 is a “barrier surface” cytokine whose expression depends on extrinsic environmental factors and when upregulated may lead to inflammatory disorders such as atopic dermatitis, psoriasis, or asthma. This review summarizes the progress of the recent years regarding the effects of IL-25 on the regulation of immune response and the balance between its homeostatic and pathogenic role in various epithelia. We revisit IL-25’s general and tissue-specific mechanisms of action, mediated signaling pathways, and transcription factors activated in immune and resident cells. 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| subjects | Asthma Atopic dermatitis Cell cycle Chemokines chronic rhinosinusitis contact dermatitis Crohn disease Cytokines Dendritic cells Eczema Environmental factors Epithelial cells Gastrointestinal tract Gene expression Homeostasis idiopathic pulmonary fibrosis IL-17E IL-25 Immunology inflammatory bowel disease Inflammatory diseases Interleukin 17 keratinocytes Kinases Lymphocytes Lymphocytes T Lymphoid cells Phosphorylation Proteins Psoriasis Pulmonary fibrosis Recruitment Rhinitis Signal transduction Sinusitis Transcription factors tuft cells ulcerative colitis |
| title | IL-25 (IL-17E) in epithelial immunology and pathophysiology |
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