Letter to the EditorPsoriasis-like skin lesions are dependent on IL-23 but develop in the absence of IL-22 in a model mouse
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Funding
This study was supported by Grant-in-Aid for Scientific Research (no. 22591242).
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Cited by (9)
Identification and functional analysis of miRNAs in N. benthamiana in response to A. longipes infection
2022, Physiological and Molecular Plant PathologyCitation Excerpt :Furthermore, ethylene levels were found to increase substantially in infected tobacco compared with uninfected (mock) plants. Ethylene signalling has been shown to play an important role in the infection process of brown spot in tobacco [9]. In addition, a large number of key genes and molecular processes have been identified during brown spot disease infection of tobacco.
Levels of the interleukins 17A, 22, and 23 and the S100 protein family in the gingival crevicular fluid of psoriatic patients with or without periodontitis
2021, Anais Brasileiros de DermatologiaCitation Excerpt :Another study showed that periodontitis seems to alter IL-17 levels in gingival tissue samples of arthritic rats.45 Regarding psoriasis, it has been reported that IL-22 and IL-23 are required to induce psoriasis-like lesions in animal models.46,47 Similarly to the present results, some studies have reported no differences in the levels of IL-22 and IL-23 in the serum of patients with psoriasis vs. those of healthy controls.48,49
Stat3 activation in epidermal keratinocytes induces Langerhans cell activation to form an essential circuit for psoriasis via IL-23 production
2019, Journal of Dermatological ScienceCitation Excerpt :These findings validate the important role of IL-23/Th17 pathway in the development of psoriasis-like lesion in K5.Stat3C mice. In addition, we have demonstrated several crucial findings in the pathogenesis of psoriasis using K5.Stat3C mice [9–14]. Langerhans cells (LCs) are the dendritic cells (DCs) that reside in the epidermal layer of the skin [15].
Oral administration of a novel RORγt antagonist attenuates psoriasis-like skin lesion of two independent mouse models through neutralization of IL-17
2017, Journal of Dermatological ScienceCitation Excerpt :Since ILC3s are involved in psoriatic lesions as found in inflammatory bowel diseases [24], it might be that ILC3s were the source of IL-22 production after treatment with A213, which affected IL-17 from Th17 cells. In contrast to the paramount therapeutic outcome of anti-IL-17A antibodies, lowering of IL-22 alone might not be beneficial for treatment of psoriasis, since clinical trial with anti-IL-22 antibody was not successful thus far and psoriasis-like lesions were not attenuated by deletion of IL22 gene [25]. It should be noted that A213 did not affect Ifng in skin lesions or SDLNs, strongly suggesting that A213 affected IL-17-producing cells, but not Th1 cells.
Human mast cells are major IL-22 producers in patients with psoriasis and atopic dermatitis
2015, Journal of Allergy and Clinical ImmunologyCitation Excerpt :Several experimental models of psoriasis, including psoriatic-like inflammation induced by imiquimod and administration of IL-23 in mice, are IL-22 dependent.37,46 However, overexpression of IL-24 in keratinocytes results in psoriasis-like skin inflammation that is not dependent on IL-22 expression because disease manifestation can be induced in IL-22–deficient mice.47,48 Very little has been published on the effects of IL-22 antagonists in patients with psoriasis.
Recent advances in atopic dermatitis and psoriasis: Genetic background, barrier function, and therapeutic targets
2015, Journal of Dermatological Science