<i>Indoleamine 2,3-Dioxygenase 2</i> Deficiency Exacerbates Imiquimod-Induced Psoriasis-Like Skin Inflammation
<i>Indoleamine 2,3-dioxygenase 1</i> (<i>IDO1</i>) is an enzyme known to suppress immune responses, and several reports have showed that it is associated with psoriasis. <i>IDO2</i> is an isoform of <i>IDO1</i>, recently identified as a catalytic enzym...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2020-08-01
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| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/21/15/5515 |
| Summary: | <i>Indoleamine 2,3-dioxygenase 1</i> (<i>IDO1</i>) is an enzyme known to suppress immune responses, and several reports have showed that it is associated with psoriasis. <i>IDO2</i> is an isoform of <i>IDO1</i>, recently identified as a catalytic enzyme in the tryptophan-kynurenine pathway, which is expressed in dendritic cells and monocytes. The expression of <i>IDO2</i> in immune cells suggests that <i>IDO2</i> may contribute to immune functions. However, the role of <i>IDO2</i> in the pathogenesis of psoriasis remains unclear. In this study, to elucidate the role of <i>IDO2</i> in psoriasis, we assessed imiquimod (IMQ)-induced psoriasis-like dermatitis in <i>IDO2</i> knockout (KO) mice. Skin inflammation, evaluated by scoring erythema, scaling, and ear thickness, was significantly worse in the <i>IDO2</i> KO mice than in the wild-type (WT) mice. The mRNA expression levels of TNF-α, IL-23p19, and IL-17A, key cytokines involved in the development of psoriasis, were also increased in the <i>IDO2</i> KO mice. Furthermore, immunohistochemistry revealed that the number of Ki67-positive cells in the epidermis and CD4-, CD8-, and IL-17-positive lymphocytes infiltrating the dermis were significantly increased in the <i>IDO2</i> KO mice. These results suggest that <i>IDO2</i> might decrease IL-17 expression, thereby resulting in the suppression of skin inflammation in IMQ-induced psoriasis-like dermatitis. |
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| ISSN: | 1661-6596 1422-0067 |