Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated
Psoriasis is a chronic inflammatory skin disease characterized by IL-17-dominant abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes, and comorbid arthritis or cardiometabolic diseases. This Special Issue presented updated informa...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-03-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/22/6/2979 |
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| author | Naoko Kanda |
| author_facet | Naoko Kanda |
| author_sort | Naoko Kanda |
| collection | DOAJ |
| description | Psoriasis is a chronic inflammatory skin disease characterized by IL-17-dominant abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes, and comorbid arthritis or cardiometabolic diseases. This Special Issue presented updated information on pathogenesis, comorbidities, and therapy of psoriasis. The pathogenesis of psoriasis may involve the dysfunction of indoleamine 2,3-dioxygenase 2 or of UBA domain containing 1-mediated regulation of CARD14/CARMA2<i>sh</i>. The blood cells of psoriasis patients showed the enhanced oxidative stress/autophagy flux and decreased 20S proteasome activity. Elafin, clusterin, or selenoprotein P may act as biomarkers for psoriasis and comorbid metabolic diseases. The proteomic profile of psoriasis lesions showed the dysfunction of dermal fibroblasts; up-regulation of proinflammatory factors and signal transduction or down-regulation of structural molecules. The skin inflammation in psoriasis may populate certain gut bacteria, such as <i>Staphylococcus aureus</i> and <i>Streptococcus danieliae,</i> which worsen the skin inflammation in turn. The psoriasis-associated pruritus may be caused by immune, nervous, or vascular mechanisms. In addition to current oral treatments and biologics, a new treatment option for psoriasis is now being developed, such as retinoic-acid-receptor-related orphan nuclear receptor γt inhibitors, IL-36 receptor antagonist, or aryl hydrocarbon receptor agonist. Antimicrobial peptides and innate immune cells, involved in the pathogenesis of psoriasis, may be novel therapeutic targets. The pathomechanisms and responses to drugs in collagen diseases are partially shared with and partially different from those in psoriasis. Certain nutrients can exacerbate or regulate the progress of psoriasis. The articles in this Special Issue will encourage attractive approaches to psoriasis by future researchers. |
| first_indexed | 2024-03-10T13:13:24Z |
| format | Article |
| id | doaj.art-55c84733156d4141a385ec7f2a4674b2 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T13:13:24Z |
| publishDate | 2021-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-55c84733156d4141a385ec7f2a4674b22023-11-21T10:34:41ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-03-01226297910.3390/ijms22062979Psoriasis: Pathogenesis, Comorbidities, and Therapy UpdatedNaoko Kanda0Department of Dermatology, Nippon Medical School Chiba Hokusoh Hospital, Inzai, Chiba 2701694, JapanPsoriasis is a chronic inflammatory skin disease characterized by IL-17-dominant abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes, and comorbid arthritis or cardiometabolic diseases. This Special Issue presented updated information on pathogenesis, comorbidities, and therapy of psoriasis. The pathogenesis of psoriasis may involve the dysfunction of indoleamine 2,3-dioxygenase 2 or of UBA domain containing 1-mediated regulation of CARD14/CARMA2<i>sh</i>. The blood cells of psoriasis patients showed the enhanced oxidative stress/autophagy flux and decreased 20S proteasome activity. Elafin, clusterin, or selenoprotein P may act as biomarkers for psoriasis and comorbid metabolic diseases. The proteomic profile of psoriasis lesions showed the dysfunction of dermal fibroblasts; up-regulation of proinflammatory factors and signal transduction or down-regulation of structural molecules. The skin inflammation in psoriasis may populate certain gut bacteria, such as <i>Staphylococcus aureus</i> and <i>Streptococcus danieliae,</i> which worsen the skin inflammation in turn. The psoriasis-associated pruritus may be caused by immune, nervous, or vascular mechanisms. In addition to current oral treatments and biologics, a new treatment option for psoriasis is now being developed, such as retinoic-acid-receptor-related orphan nuclear receptor γt inhibitors, IL-36 receptor antagonist, or aryl hydrocarbon receptor agonist. Antimicrobial peptides and innate immune cells, involved in the pathogenesis of psoriasis, may be novel therapeutic targets. The pathomechanisms and responses to drugs in collagen diseases are partially shared with and partially different from those in psoriasis. Certain nutrients can exacerbate or regulate the progress of psoriasis. The articles in this Special Issue will encourage attractive approaches to psoriasis by future researchers.https://www.mdpi.com/1422-0067/22/6/2979oxidative stressantimicrobial peptideinnate immune cellnutrientUBA domain containing 1indoleamine 2,3-dioxygenase 2 |
| spellingShingle | Naoko Kanda Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated International Journal of Molecular Sciences oxidative stress antimicrobial peptide innate immune cell nutrient UBA domain containing 1 indoleamine 2,3-dioxygenase 2 |
| title | Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated |
| title_full | Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated |
| title_fullStr | Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated |
| title_full_unstemmed | Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated |
| title_short | Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated |
| title_sort | psoriasis pathogenesis comorbidities and therapy updated |
| topic | oxidative stress antimicrobial peptide innate immune cell nutrient UBA domain containing 1 indoleamine 2,3-dioxygenase 2 |
| url | https://www.mdpi.com/1422-0067/22/6/2979 |
| work_keys_str_mv | AT naokokanda psoriasispathogenesiscomorbiditiesandtherapyupdated |