Immune regulation in pathophysiology and targeted therapy for itch in atopic dermatitis
Itch is an unpleasant perception that provokes one to desire to scratch. It results from the activation of free nerve endings by noxious stimuli in the skin. Atopic dermatitis (AD) is a prototypic inflammatory skin disease that always occurs with an intense itch. AD involves many components of skin-...
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2016-03-01
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| Series: | Dermatologica Sinica |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1027811715001123 |
| _version_ | 1819041644899467264 |
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| author | Chih-Hung Lee |
| author_facet | Chih-Hung Lee |
| author_sort | Chih-Hung Lee |
| collection | DOAJ |
| description | Itch is an unpleasant perception that provokes one to desire to scratch. It results from the activation of free nerve endings by noxious stimuli in the skin. Atopic dermatitis (AD) is a prototypic inflammatory skin disease that always occurs with an intense itch. AD involves many components of skin-associated lymphoid tissue (SALT). As a disease with polarized T helper 2 cell activation, AD involves eosinophil infiltration and immunoglobulin E, interleukin (IL)-2, IL-4, IL-13, and IL-31 production. As a disease involving an impaired skin barrier, AD is characterized by the enhanced transepidermal entry of allergens and the production of thymic stromal lymphopoietin (TSLP) from epidermal keratinocytes, which worsen atopic march and disease progression. Both immune and epidermal events interact with cutaneous nerve components, including transient receptor potential (TRP) channels and opioid receptors, causing both the perception and propagation of itch from the skin to the brain. In addition to treating itch through TRP channels and opioid receptors, it might be possible to target the various cellular components of SALT, including keratinocytes, eosinophils, and soluble factors, such as IL-31, IL-4, IL-13, IL-31, and TSLP. |
| first_indexed | 2024-12-21T09:28:17Z |
| format | Article |
| id | doaj.art-32b44c968ff44178864e4384f39fd85f |
| institution | Directory Open Access Journal |
| issn | 1027-8117 |
| language | English |
| last_indexed | 2024-12-21T09:28:17Z |
| publishDate | 2016-03-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Dermatologica Sinica |
| spelling | doaj.art-32b44c968ff44178864e4384f39fd85f2022-12-21T19:08:49ZengWolters Kluwer Medknow PublicationsDermatologica Sinica1027-81172016-03-013411510.1016/j.dsi.2015.10.002Immune regulation in pathophysiology and targeted therapy for itch in atopic dermatitisChih-Hung LeeItch is an unpleasant perception that provokes one to desire to scratch. It results from the activation of free nerve endings by noxious stimuli in the skin. Atopic dermatitis (AD) is a prototypic inflammatory skin disease that always occurs with an intense itch. AD involves many components of skin-associated lymphoid tissue (SALT). As a disease with polarized T helper 2 cell activation, AD involves eosinophil infiltration and immunoglobulin E, interleukin (IL)-2, IL-4, IL-13, and IL-31 production. As a disease involving an impaired skin barrier, AD is characterized by the enhanced transepidermal entry of allergens and the production of thymic stromal lymphopoietin (TSLP) from epidermal keratinocytes, which worsen atopic march and disease progression. Both immune and epidermal events interact with cutaneous nerve components, including transient receptor potential (TRP) channels and opioid receptors, causing both the perception and propagation of itch from the skin to the brain. In addition to treating itch through TRP channels and opioid receptors, it might be possible to target the various cellular components of SALT, including keratinocytes, eosinophils, and soluble factors, such as IL-31, IL-4, IL-13, IL-31, and TSLP.http://www.sciencedirect.com/science/article/pii/S1027811715001123atopic dermatitisIL-31itchSALTTSLP |
| spellingShingle | Chih-Hung Lee Immune regulation in pathophysiology and targeted therapy for itch in atopic dermatitis Dermatologica Sinica atopic dermatitis IL-31 itch SALT TSLP |
| title | Immune regulation in pathophysiology and targeted therapy for itch in atopic dermatitis |
| title_full | Immune regulation in pathophysiology and targeted therapy for itch in atopic dermatitis |
| title_fullStr | Immune regulation in pathophysiology and targeted therapy for itch in atopic dermatitis |
| title_full_unstemmed | Immune regulation in pathophysiology and targeted therapy for itch in atopic dermatitis |
| title_short | Immune regulation in pathophysiology and targeted therapy for itch in atopic dermatitis |
| title_sort | immune regulation in pathophysiology and targeted therapy for itch in atopic dermatitis |
| topic | atopic dermatitis IL-31 itch SALT TSLP |
| url | http://www.sciencedirect.com/science/article/pii/S1027811715001123 |
| work_keys_str_mv | AT chihhunglee immuneregulationinpathophysiologyandtargetedtherapyforitchinatopicdermatitis |