{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T15:21:53Z","timestamp":1773674513657,"version":"3.50.1"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2009,10,1]],"date-time":"2009-10-01T00:00:00Z","timestamp":1254355200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Psoriasis vulgaris is a common chronic inflammatory skin disease involving cytokines and an activated cellular immune system. At variance to skin from patients with atopic dermatitis or from healthy subjects, human psoriatic skin lesions exhibit strong activation of transcription factor NF-\u03baB that is mainly confined to dermal macrophages, whereas only a few dendritic cells but no CD3+ lymphocytes show activated NF-\u03baB. Since NF-\u03baB signaling is required for the induction and\/or function of many cytokines and aberrant cytokine expression has been proposed as an underlying cause of psoriasis, we investigated whether NF-\u03baB targeting would affect the course of the disease in the CD18 hypomorphic (CD18hypo) mouse model of psoriasis. When mice with severe psoriasiform lesions were treated systemically or locally with the I\u03baB kinase inhibitor acetyl-11-keto-\u03b2-boswellic acid (AK\u03b2BA), NF-\u03baB signaling and the subsequent NF-\u03baB-dependent cytokine production as shown by the TNF-\u03b1 production of macrophages were profoundly suppressed. Additionally, application of the compound counteracted the intradermal MCP-1, IL-12, and IL-23 expression in previously lesional skin areas, led to resolution of the abundant immune cell infiltrates, and significantly reduced the increased proliferation of the keratinocytes. Overall, the AK\u03b2BA treatment was accompanied by a profound improvement of the psoriasis disease activity score in the CD18hypo mice with reconstitution of a nearly normal phenotype within the chosen observation period. Our data demonstrate that NF-\u03baB signaling is pivotal for the pathogenesis in the CD18hypo mouse model of psoriasis. Therefore, targeting NF-\u03baB might provide an effective strategy for the treatment of psoriasis.<\/jats:p>","DOI":"10.4049\/jimmunol.0900521","type":"journal-article","created":{"date-parts":[[2009,9,15]],"date-time":"2009-09-15T01:31:13Z","timestamp":1252978273000},"page":"4755-4763","source":"Crossref","is-referenced-by-count":83,"title":["Targeting NF-\u03baB with a Natural Triterpenoid Alleviates Skin Inflammation in a Mouse Model of Psoriasis"],"prefix":"10.1093","volume":"183","author":[{"given":"Honglin","family":"Wang","sequence":"first","affiliation":[{"name":"Shanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai Jiao Tong University Medical School , Shanghai,","place":["China"]},{"name":"Department of Dermatology and Allergic Diseases"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tatiana","family":"Syrovets","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology of Natural Products and Clinical Pharmacology, Ulm University , Ulm,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel","family":"Kess","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Allergic Diseases"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Berthold","family":"B\u00fcchele","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology of Natural Products and Clinical Pharmacology, Ulm University , Ulm,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Heidi","family":"Hainzl","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Allergic Diseases"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Oleg","family":"Lunov","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology of Natural Products and Clinical Pharmacology, Ulm University , Ulm,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Johannes M","family":"Weiss","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Allergic Diseases"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karin","family":"Scharffetter-Kochanek","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Allergic Diseases"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Simmet","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology of Natural Products and Clinical Pharmacology, Ulm University , Ulm,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2009,10,1]]},"reference":[{"key":"2025032620132499300_R1","first-page":"1899","article-title":"Psoriasis.","volume-title":"N. 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