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The Stabilin\u2010mediated scavenging function is responsible for regulating the molecular composition of circulating blood in mammals. Stab1 and Stab2 have been shown to influence fibrosis in liver and kidneys and to modulate inflammation in atherosclerosis. In this context, circulating and localized TGFBi and POSTN are differentially controlled by the Stabilins as their receptors. To assess Stab1 and Stab2 functions in inflammatory and fibrotic skin disease, topical Imiquimod (IMQ) was used to induce psoriasis\u2010like skin lesions in mice and Bleomycin (BLM) was applied subcutaneously to induce scleroderma\u2010like effects in the skin. The topical treatment with IMQ, as expected, led to psoriasis\u2010like changes in the skin of mice, including increased epidermal thickness and significant weight loss. Clinical severity was reduced in Stab2\u2010deficient compared to Stab1\u2010deficient mice. We did not observe differential effects in the skin of Stabilin\u2010deficient mice after bleomycin injection. Interestingly, treatment with IMQ led to a significant increase of Stabilin ligand TGFBi plasma levels in\n                    <jats:italic>Stab2<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, treatment with BLM resulted in a significant decrease in TGFBi levels in\n                    <jats:italic>Stab1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Overall, Stab1 and Stab2 deficiency resulted in minor alterations of the disease phenotypes accompanied by alterations of circulating ligands in the blood in response to the disease models. Stabilin\u2010mediated clearance of TGFBi was altered in these disease processes. Taken together our results suggest that Stabilin deficiency\u2010associated plasma alterations may interfere with preclinical disease severity and treatment responses in patients.\n                  <\/jats:p>","DOI":"10.1002\/2211-5463.13857","type":"journal-article","created":{"date-parts":[[2024,7,1]],"date-time":"2024-07-01T00:15:20Z","timestamp":1719792920000},"page":"1455-1470","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Phenotypical and biochemical characterization of murine\u00a0psoriasiform and fibrotic skin disease models in\u00a0Stabilin\u2010deficient mice"],"prefix":"10.1002","volume":"14","author":[{"given":"Jessica","family":"Krzistetzko","sequence":"first","affiliation":[{"name":"Department of Dermatology, Venereology, and Allergology, University Medical Center and Medical Faculty Mannheim Heidelberg University  Mannheim Germany"},{"name":"Section of Clinical and Molecular Dermatology, 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