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Recombinant ISRAA ameliorates imiquimod-induced psoriasis and knocking out Israa delays its onset

Psoriasis, an inflammatory disease, is largely mediated by T-helper 17 cytokines. We have previously identified the immune system-released activating agent ( Israa ) as a novel gene that connects the nervous and immune systems. This research aims to investigate the role of the Israa gene in psoriasi...

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Bibliographic Details
Published in:Archives of dermatological research 2024-10, Vol.316 (9), p.661, Article 661
Main Authors: Alsabbagh, Manahel Mahmood, Aljishi, Muna, Sultan, Ameera, Marwani, Amar Muhsin, Althaf, Nasneen, Bakhiet, Moiz, Taha, Safa
Format: Article
Language:English
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Summary:Psoriasis, an inflammatory disease, is largely mediated by T-helper 17 cytokines. We have previously identified the immune system-released activating agent ( Israa ) as a novel gene that connects the nervous and immune systems. This research aims to investigate the role of the Israa gene in psoriasis in vivo using the imiquimod-induced psoriasis model. We established the model in C57BL/6 wildtype mice, which were then treated with 200 pg/mouse, 400 pg/mouse, or 800 pg/mouse of recombinant ISRAA compared to methotrexate. Subsequently, we also induced psoriasis in Israa -knockout mice to confirm the effect of Israa . Results consistently showed improvement in psoriasis in all groups receiving recombinant ISRAA. The 200 pg/mouse dose eliminated the disease, reduced the cutaneous release of IL-17 to one-third and TNF-α to one-sixth, increased IL-10 release to over 500 pg, completely resolved parakeratosis, decreased epidermal thickness to one-half, and reduced the expression of CD4 and neutrophil elastase in the skin (all p  
ISSN:1432-069X
0340-3696
1432-069X
DOI:10.1007/s00403-024-03410-5